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Journal articles on the topic 'Cellular bioenergetics'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Hill, Bradford G., Gloria A. Benavides, Jack R. Lancaster, Scott Ballinger, Lou Dell’Italia, Jianhua Zhang, and Victor M. Darley-Usmar. "Integration of cellular bioenergetics with mitochondrial quality control and autophagy." Biological Chemistry 393, no. 12 (December 1, 2012): 1485–512. http://dx.doi.org/10.1515/hsz-2012-0198.

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Abstract Bioenergetic dysfunction is emerging as a cornerstone for establishing a framework for understanding the pathophysiology of cardiovascular disease, diabetes, cancer and neurodegeneration. Recent advances in cellular bioenergetics have shown that many cells maintain a substantial bioenergetic reserve capacity, which is a prospective index of ‘healthy’ mitochondrial populations. The bioenergetics of the cell are likely regulated by energy requirements and substrate availability. Additionally, the overall quality of the mitochondrial population and the relative abundance of mitochondria in cells and tissues also impinge on overall bioenergetic capacity and resistance to stress. Because mitochondria are susceptible to damage mediated by reactive oxygen/nitrogen and lipid species, maintaining a ‘healthy’ population of mitochondria through quality control mechanisms appears to be essential for cell survival under conditions of pathological stress. Accumulating evidence suggest that mitophagy is particularly important for preventing amplification of initial oxidative insults, which otherwise would further impair the respiratory chain or promote mutations in mitochondrial DNA (mtDNA). The processes underlying the regulation of mitophagy depend on several factors, including the integrity of mtDNA, electron transport chain activity, and the interaction and regulation of the autophagic machinery. The integration and interpretation of cellular bioenergetics in the context of mitochondrial quality control and genetics is the theme of this review.

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Augsburger, Fiona, Elisa B. Randi, Mathieu Jendly, Kelly Ascencao, Nahzli Dilek, and Csaba Szabo. "Role of 3-Mercaptopyruvate Sulfurtransferase in the Regulation of Proliferation, Migration, and Bioenergetics in Murine Colon Cancer Cells." Biomolecules 10, no. 3 (March 13, 2020): 447. http://dx.doi.org/10.3390/biom10030447.

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3-mercaptopyruvate sulfurtransferase (3-MST) has emerged as one of the significant sources of biologically active sulfur species in various mammalian cells. The current study was designed to investigate the functional role of 3-MST’s catalytic activity in the murine colon cancer cell line CT26. The novel pharmacological 3-MST inhibitor HMPSNE was used to assess cancer cell proliferation, migration and bioenergetics in vitro. Methods included measurements of cell viability (MTT and LDH assays), cell proliferation and in vitro wound healing (IncuCyte) and cellular bioenergetics (Seahorse extracellular flux analysis). 3-MST expression was detected by Western blotting; H2S production was measured by the fluorescent dye AzMC. The results show that CT26 cells express 3-MST protein and mRNA, as well as several enzymes involved in H2S degradation (TST, ETHE1). Pharmacological inhibition of 3-MST concentration-dependently suppressed H2S production and, at 100 and 300 µM, attenuated CT26 proliferation and migration. HMPSNE exerted a bell-shaped effect on several cellular bioenergetic parameters related to oxidative phosphorylation, while other bioenergetic parameters were either unaffected or inhibited at the highest concentration of the inhibitor tested (300 µM). In contrast to 3-MST, the expression of CBS (another H2S producing enzyme which has been previously implicated in the regulation of various biological parameters in other tumor cells) was not detectable in CT26 cells and pharmacological inhibition of CBS exerted no significant effects on CT26 proliferation or bioenergetics. In summary, 3-MST catalytic activity significantly contributes to the regulation of cellular proliferation, migration and bioenergetics in CT26 murine colon cancer cells. The current studies identify 3-MST as the principal source of biologically active H2S in this cell line.

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Lehrer, H. Matthew, Lauren Chu, Martica Hall, and Kyle Murdock. "009 Self-Reported Sleep Efficiency and Duration are Associated with Systemic Bioenergetic Function in Community-Dwelling Adults." Sleep 44, Supplement_2 (May 1, 2021): A4. http://dx.doi.org/10.1093/sleep/zsab072.008.

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Abstract Introduction Sleep is important for aging, health, and disease, but its cellular role in these outcomes is poorly understood. Basic research suggests that disturbed and insufficient sleep impair mitochondrial bioenergetics, which is involved in numerous aging-related chronic conditions. However, the relationship between sleep and bioenergetics has not been examined in humans. We examined associations of self-reported sleep with systemic bioenergetic function in peripheral blood mononuclear cells (PBMCs) of community-dwelling adults. Methods N = 43 adults (79% female) ages 48–70 (M = 61.63, SD = 5.99) completed the Pittsburgh Sleep Quality Index (PSQI) from which key components of sleep (satisfaction, alertness, timing, efficiency, and duration) were calculated. Participants provided blood samples from which PBMCs were isolated and measured for bioenergetics using extracellular flux analysis. Associations of sleep components with bioenergetic parameters, including the Bioenergetic Health Index (BHI), were examined. Results In bivariate analyses, lower sleep efficiency was associated with lower maximal respiration, spare capacity, and BHI (ps < 0.05). Longer sleep duration was associated with lower BHI (p < 0.01) and later sleep timing was associated with higher basal respiration, ATP-linked respiration, maximal respiration, spare capacity, and non-mitochondrial respiration (ps < 0.05). After adjustment for age, sex, and body mass index, lower sleep efficiency (β = 0.52, p < 0.01) and longer sleep duration (β = -0.43, p < 0.01) were associated with lower BHI. Conclusion Self-reported indices of sleep efficiency and duration are related to systemic bioenergetic function in humans, suggesting a possible cellular pathway linking sleep to health. Support (if any) T32HL082610

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Welch, G. R. "Bioenergetics and the cellular microenvironment." Pure and Applied Chemistry 65, no. 9 (January 1, 1993): 1907–14. http://dx.doi.org/10.1351/pac199365091907.

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Acuña-Castroviejo, Darío, Miguel Martín, Manuel Macías, Germaine Escames, Josefa León, Huda Khaldy, and Russel J. Reiter. "Melatonin, mitochondria, and cellular bioenergetics." Journal of Pineal Research 30, no. 2 (March 2001): 65–74. http://dx.doi.org/10.1034/j.1600-079x.2001.300201.x.

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6

Heiden, Matthew Vander. "Cellular Bioenergetics in Lymphoid Neoplasia." Blood 118, no. 21 (November 18, 2011): SCI—25—SCI—25. http://dx.doi.org/10.1182/blood.v118.21.sci-25.sci-25.

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Abstract Abstract SCI-25 Many cancer cells metabolize glucose by aerobic glycolysis, a phenomenon characterized by increased glycolysis with lactate production and decreased oxidative phosphorylation. We have argued that alterations in cell metabolism associated with cancer may be selected by cancer cells to meet the distinct metabolic needs of proliferation. Unlike metabolism in differentiated cells, which is geared toward efficient ATP generation, the metabolism in cancer cells must be adapted to facilitate the accumulation of biomass. Cancer cells divert a larger fraction of their nutrient metabolism to pathways other than mitochondrial respiration regardless of oxygen availability. Nevertheless, oxygen levels still influence how nutrients are metabolized. We have found that the source of carbon used in various anabolic processes varies based on oxygen levels. Furthermore, the enzymes used to metabolize nutrients can also differ based on the cellular context. This includes regulation of isocitrate dehydrogenase, an enzyme that is mutated in some cancers. There is also strong selection for use of the M2 isoform of pyruvate kinase (PK-M2) to metabolize glucose in cancer cell lines. However, evidence from mouse models suggests that PK-M2 is dispensable for glucose metabolism by many tumors in vivo, suggesting an alternate pathway to convert phosphoenolpyruvate to pyruvate can be used to metabolize glucose. This regulation of pyruvate kinase also plays an important role in hematopoietic stem cell biology. Together, these findings argue that distinct metabolic phenotypes exist among proliferating cells, and both environmental and genetic factors influence how metabolism is regulated to support cell growth. Disclosures: Vander Heiden: Agios Pharmaceuticals: Consultancy, Equity Ownership.

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Davies, Karen M., and Bertram Daum. "Role of cryo-ET in membrane bioenergetics research." Biochemical Society Transactions 41, no. 5 (September 23, 2013): 1227–34. http://dx.doi.org/10.1042/bst20130029.

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To truly understand bioenergetic processes such as ATP synthesis, membrane-bound substrate transport or flagellar rotation, systems need to be analysed in a cellular context. Cryo-ET (cryo-electron tomography) is an essential part of this process, as it is currently the only technique which can directly determine the spatial organization of proteins at the level of both the cell and the individual protein complexes. The need to assess bioenergetic processes at a cellular level is becoming more and more apparent with the increasing interest in mitochondrial diseases. In recent years, cryo-ET has contributed significantly to our understanding of the molecular organization of mitochondria and chloroplasts. The present mini-review first describes the technique of cryo-ET and then discusses its role in membrane bioenergetics specifically in chloroplasts and mitochondrial research.

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Chacko, Balu K., Philip A. Kramer, Saranya Ravi, Gloria A. Benavides, Tanecia Mitchell, Brian P. Dranka, David Ferrick, et al. "The Bioenergetic Health Index: a new concept in mitochondrial translational research." Clinical Science 127, no. 6 (May 29, 2014): 367–73. http://dx.doi.org/10.1042/cs20140101.

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Bioenergetics has become central to our understanding of pathological mechanisms, the development of new therapeutic strategies and as a biomarker for disease progression in neurodegeneration, diabetes, cancer and cardiovascular disease. A key concept is that the mitochondrion can act as the ‘canary in the coal mine’ by serving as an early warning of bioenergetic crisis in patient populations. We propose that new clinical tests to monitor changes in bioenergetics in patient populations are needed to take advantage of the early and sensitive ability of bioenergetics to determine severity and progression in complex and multifactorial diseases. With the recent development of high-throughput assays to measure cellular energetic function in the small number of cells that can be isolated from human blood these clinical tests are now feasible. We have shown that the sequential addition of well-characterized inhibitors of oxidative phosphorylation allows a bioenergetic profile to be measured in cells isolated from normal or pathological samples. From these data we propose that a single value–the Bioenergetic Health Index (BHI)–can be calculated to represent the patient's composite mitochondrial profile for a selected cell type. In the present Hypothesis paper, we discuss how BHI could serve as a dynamic index of bioenergetic health and how it can be measured in platelets and leucocytes. We propose that, ultimately, BHI has the potential to be a new biomarker for assessing patient health with both prognostic and diagnostic value.

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Narchi, Hassib, Pramathan Thachillath, and Abdul-Kader Souid. "Forebrain cellular bioenergetics in neonatal mice." Journal of Neonatal-Perinatal Medicine 11, no. 1 (April 16, 2018): 79–86. http://dx.doi.org/10.3233/npm-181737.

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Acin-Perez, Rebeca, Cristiane Benincá, Byourak Shabane, Orian S. Shirihai, and Linsey Stiles. "Utilization of Human Samples for Assessment of Mitochondrial Bioenergetics: Gold Standards, Limitations, and Future Perspectives." Life 11, no. 9 (September 10, 2021): 949. http://dx.doi.org/10.3390/life11090949.

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Mitochondrial bioenergetic function is a central component of cellular metabolism in health and disease. Mitochondrial oxidative phosphorylation is critical for maintaining energetic homeostasis, and impairment of mitochondrial function underlies the development and progression of metabolic diseases and aging. However, measurement of mitochondrial bioenergetic function can be challenging in human samples due to limitations in the size of the collected sample. Furthermore, the collection of samples from human cohorts is often spread over multiple days and locations, which makes immediate sample processing and bioenergetics analysis challenging. Therefore, sample selection and choice of tests should be carefully considered. Basic research, clinical trials, and mitochondrial disease diagnosis rely primarily on skeletal muscle samples. However, obtaining skeletal muscle biopsies requires an appropriate clinical setting and specialized personnel, making skeletal muscle a less suitable tissue for certain research studies. Circulating white blood cells and platelets offer a promising primary tissue alternative to biopsies for the study of mitochondrial bioenergetics. Recent advances in frozen respirometry protocols combined with the utilization of minimally invasive and non-invasive samples may provide promise for future mitochondrial research studies in humans. Here we review the human samples commonly used for the measurement of mitochondrial bioenergetics with a focus on the advantages and limitations of each sample.

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Gevezova, Maria, Danail Minchev, Iliana Pacheva, Yordan Sbirkov, Ralitsa Yordanova, Elena Timova, Vasil Kotetarov, Ivan Ivanov, and Victoria Sarafian. "Cellular Bioenergetic and Metabolic Changes in Patients with Autism Spectrum Disorder." Current Topics in Medicinal Chemistry 21, no. 11 (August 4, 2021): 985–94. http://dx.doi.org/10.2174/1568026621666210521142131.

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Background: Although Autism Spectrum Disorder (ASD) is considered a heterogeneous neurological disease in childhood, a growing body of evidence associates it with mitochondrial dysfunction explaining the observed comorbidities. Introduction: The aim of this study is to identify variations in cellular bioenergetics and metabolism dependent on mitochondrial function in ASD patients and healthy controls using Peripheral Blood Mononuclear Cells (PBMCs). We hypothesized that PBMCs may reveal the cellular pathology and provide evidence of bioenergetic and metabolic changes accompanying the disease. Method: PBMC from children with ASD and a control group of the same age and gender were isolated. All patients underwent an in-depth clinical evaluation. A well-characterized cohort of Bulgarian children is selected. Bioenergetic and metabolic studies of isolated PBMCs are performed with a Seahorse XFp analyzer. Result: Our data show that PBMCs from patients with ASD have increased respiratory reserve capacity (by 27.5%), increased maximal respiration (by 67%) and altered adaptive response to oxidative stress induced by DMNQ. In addition, we demonstrate а strong dependence on fatty acids and impaired ability to reprogram cell metabolism. The listed characteristics are not observed in the control group. These results can contribute to a better understanding of the underlying causes of ASD, which is crucial for selecting a successful treatment. Conclusion: The current study, for the first time, provides a functional analysis of cell bioenergetics and metabolic changes in a group of Bulgarian patients with ASD. It reveals physiological abnormalities that do not allow mitochondria to adapt and meet the increased energetic requirements of the cell. The link between mitochondria and ASD is not yet fully understood, but this may lead to the discovery of new approaches for nutrition and therapy.

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Liu, Haoming, Yingying Du, Jean-Philippe St-Pierre, Mads S. Bergholt, Hélène Autefage, Jianglin Wang, Mingle Cai, Gaojie Yang, Molly M. Stevens, and Shengmin Zhang. "Bioenergetic-active materials enhance tissue regeneration by modulating cellular metabolic state." Science Advances 6, no. 13 (March 2020): eaay7608. http://dx.doi.org/10.1126/sciadv.aay7608.

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Cellular bioenergetics (CBE) plays a critical role in tissue regeneration. Physiologically, an enhanced metabolic state facilitates anabolic biosynthesis and mitosis to accelerate regeneration. However, the development of approaches to reprogram CBE, toward the treatment of substantial tissue injuries, has been limited thus far. Here, we show that induced repair in a rabbit model of weight-bearing bone defects is greatly enhanced using a bioenergetic-active material (BAM) scaffold compared to commercialized poly(lactic acid) and calcium phosphate ceramic scaffolds. This material was composed of energy-active units that can be released in a sustained degradation-mediated fashion once implanted. By establishing an intramitochondrial metabolic bypass, the internalized energy-active units significantly elevate mitochondrial membrane potential (ΔΨm) to supply increased bioenergetic levels and accelerate bone formation. The ready-to-use material developed here represents a highly efficient and easy-to-implement therapeutic approach toward tissue regeneration, with promise for bench-to-bedside translation.

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Padhi, Abinash, Alexander H. Thomson, Justin B. Perry, Grace N. Davis, Ryan P. McMillan, Sandra Loesgen, Elizabeth N. Kaweesa, Rakesh Kapania, Amrinder S. Nain, and David A. Brown. "Bioenergetics underlying single-cell migration on aligned nanofiber scaffolds." American Journal of Physiology-Cell Physiology 318, no. 3 (March 1, 2020): C476—C485. http://dx.doi.org/10.1152/ajpcell.00221.2019.

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Cell migration is centrally involved in a myriad of physiological processes, including morphogenesis, wound healing, tissue repair, and metastatic growth. The bioenergetics that underlie migratory behavior are not fully understood, in part because of variations in cell culture media and utilization of experimental cell culture systems that do not model physiological connective extracellular fibrous networks. In this study, we evaluated the bioenergetics of C2C12 myoblast migration and force production on fibronectin-coated nanofiber scaffolds of controlled diameter and alignment, fabricated using a nonelectrospinning spinneret-based tunable engineered parameters (STEP) platform. The contribution of various metabolic pathways to cellular migration was determined using inhibitors of cellular respiration, ATP synthesis, glycolysis, or glucose uptake. Despite immediate effects on oxygen consumption, mitochondrial inhibition only modestly reduced cell migration velocity, whereas inhibitors of glycolysis and cellular glucose uptake led to striking decreases in migration. The migratory metabolic sensitivity was modifiable based on the substrates present in cell culture media. Cells cultured in galactose (instead of glucose) showed substantial migratory sensitivity to mitochondrial inhibition. We used nanonet force microscopy to determine the bioenergetic factors responsible for single-cell force production and observed that neither mitochondrial nor glycolytic inhibition altered single-cell force production. These data suggest that myoblast migration is heavily reliant on glycolysis in cells grown in conventional media. These studies have wide-ranging implications for the causes, consequences, and putative therapeutic treatments aimed at cellular migration.

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Riddle, Ryan C., and Thomas L. Clemens. "Bone Cell Bioenergetics and Skeletal Energy Homeostasis." Physiological Reviews 97, no. 2 (April 2017): 667–98. http://dx.doi.org/10.1152/physrev.00022.2016.

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The rising incidence of metabolic diseases worldwide has prompted renewed interest in the study of intermediary metabolism and cellular bioenergetics. The application of modern biochemical methods for quantitating fuel substrate metabolism with advanced mouse genetic approaches has greatly increased understanding of the mechanisms that integrate energy metabolism in the whole organism. Examination of the intermediary metabolism of skeletal cells has been sparked by a series of unanticipated observations in genetically modified mice that suggest the existence of novel endocrine pathways through which bone cells communicate their energy status to other centers of metabolic control. The recognition of this expanded role of the skeleton has in turn led to new lines of inquiry directed at defining the fuel requirements and bioenergetic properties of bone cells. This article provides a comprehensive review of historical and contemporary studies on the metabolic properties of bone cells and the mechanisms that control energy substrate utilization and bioenergetics. Special attention is devoted to identifying gaps in our current understanding of this new area of skeletal biology that will require additional research to better define the physiological significance of skeletal cell bioenergetics in human health and disease.

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Ostojic, Sergej M. "Tackling guanidinoacetic acid for advanced cellular bioenergetics." Nutrition 34 (February 2017): 55–57. http://dx.doi.org/10.1016/j.nut.2016.09.010.

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Hertz, Leif. "Bioenergetics of cerebral ischemia: A cellular perspective." Neuropharmacology 55, no. 3 (September 2008): 289–309. http://dx.doi.org/10.1016/j.neuropharm.2008.05.023.

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Pundik, S., K. Xu, and S. Sundararajan. "Reperfusion brain injury: Focus on cellular bioenergetics." Neurology 79, Issue 13, Supplement 1 (September 24, 2012): S44—S51. http://dx.doi.org/10.1212/wnl.0b013e3182695a14.

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Stein, Asaf, Zhengkuan Mao, Angela Betancourt, and Shannon Bailey. "Effect of Hydrogen Sulfide On Cellular Bioenergetics." Free Radical Biology and Medicine 51 (November 2011): S140. http://dx.doi.org/10.1016/j.freeradbiomed.2011.10.299.

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Mishra, Jay S., Chellakkan S. Blesson, and Sathish Kumar. "Testosterone Decreases Placental Mitochondrial Content and Cellular Bioenergetics." Biology 9, no. 7 (July 20, 2020): 176. http://dx.doi.org/10.3390/biology9070176.

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Placental mitochondrial dysfunction plays a central role in the pathogenesis of preeclampsia. Since preeclampsia is a hyperandrogenic state, we hypothesized that elevated maternal testosterone levels induce damage to placental mitochondria and decrease bioenergetic profiles. To test this hypothesis, pregnant Sprague–Dawley rats were injected with vehicle or testosterone propionate (0.5 mg/kg/day) from gestation day (GD) 15 to 19. On GD20, the placentas were isolated to assess mitochondrial structure, copy number, ATP/ADP ratio, and biogenesis (Pgc-1α and Nrf1). In addition, in vitro cultures of human trophoblasts (HTR-8/SVneo) were treated with dihydrotestosterone (0.3, 1.0, and 3.0 nM), and bioenergetic profiles using seahorse analyzer were assessed. Testosterone exposure in pregnant rats led to a 2-fold increase in plasma testosterone levels with an associated decrease in placental and fetal weights compared with controls. Elevated maternal testosterone levels induced structural damage to the placental mitochondria and decreased mitochondrial copy number. The ATP/ADP ratio was reduced with a parallel decrease in the mRNA and protein expression of Pgc-1α and Nrf1 in the placenta of testosterone-treated rats compared with controls. In cultured trophoblasts, dihydrotestosterone decreased the mitochondrial copy number and reduced PGC-1α, NRF1 mRNA, and protein levels without altering the expression of mitochondrial fission/fusion genes. Dihydrotestosterone exposure induced significant mitochondrial energy deficits with a dose-dependent decrease in basal respiration, ATP-linked respiration, maximal respiration, and spare respiratory capacity. In summary, our study suggests that the placental mitochondrial dysfunction induced by elevated maternal testosterone might be a potential mechanism linking preeclampsia to feto-placental growth restriction.

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Singal, Ashwani K., Balu Chacko, Sumant Arora, Degui Zhi, and Victor Darley-Usmar. "Cellular Bioenergetics: Personalizing Treatment in Alcoholic Liver Disease." Gastroenterology 152, no. 5 (April 2017): S1112. http://dx.doi.org/10.1016/s0016-5085(17)33747-2.

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BRAUTBAR, N., K. ANDERSON, M. MAGGOTT, and S. G. MASSRY. "Magnesium depletion: myocardial cellular bioenergetics and phospholipid metabolism." Biochemical Society Transactions 13, no. 1 (February 1, 1985): 213–14. http://dx.doi.org/10.1042/bst0130213a.

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Tseng, Yu-Hua, Aaron M. Cypess, and C. Ronald Kahn. "Cellular bioenergetics as a target for obesity therapy." Nature Reviews Drug Discovery 9, no. 6 (June 2010): 465–82. http://dx.doi.org/10.1038/nrd3138.

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Tran, Kenneth, Denis S. Loiselle, and Edmund J. Crampin. "Regulation of cardiac cellular bioenergetics: mechanisms and consequences." Physiological Reports 3, no. 7 (July 2015): e12464. http://dx.doi.org/10.14814/phy2.12464.

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Abou-Hamdan, Abbas, Céline Ransy, Thomas Roger, Hala Guedouari-Bounihi, Erwan Galardon, and Frédéric Bouillaud. "Mitochondrial sulfide bioenergetics and cellular affinity for oxygen." Biochimica et Biophysica Acta (BBA) - Bioenergetics 1857 (August 2016): e73. http://dx.doi.org/10.1016/j.bbabio.2016.04.168.

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Szczepanowska, Joanna, Dominika Malinska, Mariusz R. Wieckowski, and Jerzy Duszynski. "Effect of mtDNA point mutations on cellular bioenergetics." Biochimica et Biophysica Acta (BBA) - Bioenergetics 1817, no. 10 (October 2012): 1740–46. http://dx.doi.org/10.1016/j.bbabio.2012.02.028.

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Szczepanowska, J., D. Malinska, M. R. Wieckowski, and J. Duszynski. "Effect of mtDNA point mutations on cellular bioenergetics." Biochimica et Biophysica Acta (BBA) - Bioenergetics 1817 (October 2012): S31. http://dx.doi.org/10.1016/j.bbabio.2012.06.093.

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Ferrick, David A., Andy Neilson, and Craig Beeson. "Advances in measuring cellular bioenergetics using extracellular flux." Drug Discovery Today 13, no. 5-6 (March 2008): 268–74. http://dx.doi.org/10.1016/j.drudis.2007.12.008.

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Serbulea, Vlad, Clint M. Upchurch, Michael S. Schappe, Paxton Voigt, Dory E. DeWeese, Bimal N. Desai, Akshaya K. Meher, and Norbert Leitinger. "Macrophage phenotype and bioenergetics are controlled by oxidized phospholipids identified in lean and obese adipose tissue." Proceedings of the National Academy of Sciences 115, no. 27 (June 11, 2018): E6254—E6263. http://dx.doi.org/10.1073/pnas.1800544115.

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Adipose tissue macrophages (ATMs) adapt their metabolic phenotype either to maintain lean tissue homeostasis or drive inflammation and insulin resistance in obesity. However, the factors in the adipose tissue microenvironment that control ATM phenotypic polarization and bioenergetics remain unknown. We have recently shown that oxidized phospholipids (OxPL) uniquely regulate gene expression and cellular metabolism in Mox macrophages, but the presence of the Mox phenotype in adipose tissue has not been reported. Here we show, using extracellular flux analysis, that ATMs isolated from lean mice are metabolically inhibited. We identify a unique population of CX3CR1neg/F4/80low ATMs that resemble the Mox (Txnrd1+HO1+) phenotype to be the predominant ATM phenotype in lean adipose tissue. In contrast, ATMs isolated from obese mice had characteristics typical of the M1/M2 (CD11c+CD206+) phenotype with highly activated bioenergetics. Quantifying individual OxPL species in the stromal vascular fraction of murine adipose tissue, using targeted liquid chromatography-mass spectrometry, revealed that high fat diet-induced adipose tissue expansion led to a disproportional increase in full-length over truncated OxPL species. In vitro studies showed that macrophages respond to truncated OxPL species by suppressing bioenergetics and up-regulating antioxidant programs, mimicking the Mox phenotype of ATMs isolated from lean mice. Conversely, full-length OxPL species induce proinflammatory gene expression and an activated bioenergetic profile that mimics ATMs isolated from obese mice. Together, these data identify a redox-regulatory Mox macrophage phenotype to be predominant in lean adipose tissue and demonstrate that individual OxPL species that accumulate in adipose tissue instruct ATMs to adapt their phenotype and bioenergetic profile to either maintain redox homeostasis or to promote inflammation.

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Vink, R., P. S. Portoghese, and A. I. Faden. "kappa-Opioid antagonist improves cellular bioenergetics and recovery after traumatic brain injury." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 261, no. 6 (December 1, 1991): R1527—R1532. http://dx.doi.org/10.1152/ajpregu.1991.261.6.r1527.

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Treatment with opioid receptor antagonists improves outcome after experimental brain trauma, although the mechanisms underlying the protective actions of these compounds remain speculative. We have proposed that endogenous opioids contribute to the pathophysiology of traumatic brain injury through actions at kappa-opioid receptors, possibly by affecting cellular bioenergetic state. In the present study, the effects of the kappa-selective opioid-receptor antagonist nor-binaltorphimine (nor-BNI) were examined after fluid percussion brain injury in rats. Metabolic changes were evaluated by 31P magnetic resonance spectroscopy; the same animals were subsequently followed over 2 wk to evaluate neurological recovery. Nor-BNI, administered intravenously as a 10 or 20 mg/kg bolus at 30 min after injury, significantly improved neurological outcome at 2 wk posttrauma compared with controls. Animals treated with nor-BNI showed significantly greater recovery of intracellular free magnesium concentrations and cytosolic phosphorylation potentials during the first 4 h after injury compared with saline-treated controls. The improvement in cytosolic phosphorylation potential was significantly correlated to neurological outcome. These data support the hypothesis that kappa-opioid receptors mediate pathophysiological changes after traumatic brain injury and that the beneficial effects of opioid-receptor antagonist may result from improvement of posttraumatic cellular bioenergetics.

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Mishra, Prashant, and David C. Chan. "Metabolic regulation of mitochondrial dynamics." Journal of Cell Biology 212, no. 4 (February 8, 2016): 379–87. http://dx.doi.org/10.1083/jcb.201511036.

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Mitochondria are renowned for their central bioenergetic role in eukaryotic cells, where they act as powerhouses to generate adenosine triphosphate from oxidation of nutrients. At the same time, these organelles are highly dynamic and undergo fusion, fission, transport, and degradation. Each of these dynamic processes is critical for maintaining a healthy mitochondrial population. Given the central metabolic function of mitochondria, it is not surprising that mitochondrial dynamics and bioenergetics reciprocally influence each other. We review the dynamic properties of mitochondria, with an emphasis on how these processes respond to cellular signaling events and how they affect metabolism.

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Valenti, Daniela, and Anna Atlante. "Mitochondrial Bioenergetics in Different Pathophysiological Conditions." International Journal of Molecular Sciences 22, no. 14 (July 15, 2021): 7562. http://dx.doi.org/10.3390/ijms22147562.

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Ozawa, Takayuki. "Oxidative Damage and Fragmentation of Mitochondrial DNA in Cellular Apoptosis." Bioscience Reports 17, no. 3 (June 1, 1997): 237–50. http://dx.doi.org/10.1023/a:1027324410022.

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Shangguan, Fugen, Yan Liu, Li Ma, Guiwu Qu, Qing Lv, Jing An, Shude Yang, Bin Lu, and Qizhi Cao. "Niclosamide inhibits ovarian carcinoma growth by interrupting cellular bioenergetics." Journal of Cancer 11, no. 12 (2020): 3454–66. http://dx.doi.org/10.7150/jca.41418.

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Reily, Colin, Tanecia Mitchell, Balu K. Chacko, Gloria A. Benavides, Michael P. Murphy, and Victor M. Darley-Usmar. "Mitochondrially targeted compounds and their impact on cellular bioenergetics." Redox Biology 1, no. 1 (2013): 86–93. http://dx.doi.org/10.1016/j.redox.2012.11.009.

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Grimm, A., A. G. Mensah-Nyagan, and A. Eckert. "P.1.015 Effects of neuroactive steroids on cellular bioenergetics." European Neuropsychopharmacology 24 (March 2014): S15—S16. http://dx.doi.org/10.1016/s0924-977x(14)70017-3.

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Marrades, R. M., J. Alonso, J. Roca, J. M. González de Suso, J. M. Campistol, J. A. Barberá, O. Diaz, et al. "Cellular bioenergetics after erythropoietin therapy in chronic renal failure." Journal of Clinical Investigation 97, no. 9 (May 1, 1996): 2101–10. http://dx.doi.org/10.1172/jci118647.

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Andrzejewski, Sylvia, Simon-Pierre Gravel, Michael Pollak, and Julie St-Pierre. "Metformin directly acts on mitochondria to alter cellular bioenergetics." Cancer & Metabolism 2, no. 1 (2014): 12. http://dx.doi.org/10.1186/2049-3002-2-12.

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Xu, W., T. Koeck, A. R. Lara, D. Neumann, F. P. DiFilippo, M. Koo, A. J. Janocha, et al. "Alterations of cellular bioenergetics in pulmonary artery endothelial cells." Proceedings of the National Academy of Sciences 104, no. 4 (January 16, 2007): 1342–47. http://dx.doi.org/10.1073/pnas.0605080104.

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Giorgio, Valentina, Valeria Petronilli, Maurizio Prato, Anna Ghelli, Michela Rugolo, and Paolo Bernardi. "The Effects of Idebenone on Mitochondrial and Cellular Bioenergetics." Biophysical Journal 100, no. 3 (February 2011): 46a. http://dx.doi.org/10.1016/j.bpj.2010.12.450.

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Ostojic, Sergej M. "Cellular bioenergetics of guanidinoacetic acid: the role of mitochondria." Journal of Bioenergetics and Biomembranes 47, no. 5 (August 9, 2015): 369–72. http://dx.doi.org/10.1007/s10863-015-9619-7.

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Hill, Bradford G., Sruti Shiva, Scott Ballinger, Jianhua Zhang, and Victor M. Darley-Usmar. "Bioenergetics and translational metabolism: implications for genetics, physiology and precision medicine." Biological Chemistry 401, no. 1 (December 18, 2019): 3–29. http://dx.doi.org/10.1515/hsz-2019-0268.

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AbstractIt is now becoming clear that human metabolism is extremely plastic and varies substantially between healthy individuals. Understanding the biochemistry that underlies this physiology will enable personalized clinical interventions related to metabolism. Mitochondrial quality control and the detailed mechanisms of mitochondrial energy generation are central to understanding susceptibility to pathologies associated with aging including cancer, cardiac and neurodegenerative diseases. A precision medicine approach is also needed to evaluate the impact of exercise or caloric restriction on health. In this review, we discuss how technical advances in assessing mitochondrial genetics, cellular bioenergetics and metabolomics offer new insights into developing metabolism-based clinical tests and metabolotherapies. We discuss informatics approaches, which can define the bioenergetic-metabolite interactome and how this can help define healthy energetics. We propose that a personalized medicine approach that integrates metabolism and bioenergetics with physiologic parameters is central for understanding the pathophysiology of diseases with a metabolic etiology. New approaches that measure energetics and metabolomics from cells isolated from human blood or tissues can be of diagnostic and prognostic value to precision medicine. This is particularly significant with the development of new metabolotherapies, such as mitochondrial transplantation, which could help treat complex metabolic diseases.

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Wright, JaLessa N., Gloria A. Benavides, Michelle S. Johnson, Willayat Wani, Xiaosen Ouyang, Luyun Zou, Helen E. Collins, Jianhua Zhang, Victor Darley-Usmar, and John C. Chatham. "Acute increases in O-GlcNAc indirectly impair mitochondrial bioenergetics through dysregulation of LonP1-mediated mitochondrial protein complex turnover." American Journal of Physiology-Cell Physiology 316, no. 6 (June 1, 2019): C862—C875. http://dx.doi.org/10.1152/ajpcell.00491.2018.

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The attachment of O-linked β- N-acetylglucosamine ( O-GlcNAc) to the serine and threonine residues of proteins in distinct cellular compartments is increasingly recognized as an important mechanism regulating cellular function. Importantly, the O-GlcNAc modification of mitochondrial proteins has been identified as a potential mechanism to modulate metabolism under stress with both potentially beneficial and detrimental effects. This suggests that temporal and dose-dependent changes in O-GlcNAcylation may have different effects on mitochondrial function. In the current study, we found that acutely augmenting O-GlcNAc levels by inhibiting O-GlcNAcase with Thiamet-G for up to 6 h resulted in a time-dependent decrease in cellular bioenergetics and decreased mitochondrial complex I, II, and IV activities. Under these conditions, mitochondrial number was unchanged, whereas an increase in the protein levels of the subunits of several electron transport complex proteins was observed. However, the observed bioenergetic changes appeared not to be due to direct increased O-GlcNAc modification of complex subunit proteins. Increases in O-GlcNAc were also associated with an accumulation of mitochondrial ubiquitinated proteins; phosphatase and tensin homolog induced kinase 1 (PINK1) and p62 protein levels were also significantly increased. Interestingly, the increase in O-GlcNAc levels was associated with a decrease in the protein levels of the mitochondrial Lon protease homolog 1 (LonP1), which is known to target complex IV subunits and PINK1, in addition to other mitochondrial proteins. These data suggest that impaired bioenergetics associated with short-term increases in O-GlcNAc levels could be due to impaired, LonP1-dependent, mitochondrial complex protein turnover.

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Puurand, Marju, Kersti Tepp, Natalja Timohhina, Jekaterina Aid, Igor Shevchuk, Vladimir Chekulayev, and Tuuli Kaambre. "Tubulin βII and βIII Isoforms as the Regulators of VDAC Channel Permeability in Health and Disease." Cells 8, no. 3 (March 13, 2019): 239. http://dx.doi.org/10.3390/cells8030239.

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In recent decades, there have been several models describing the relationships between the cytoskeleton and the bioenergetic function of the cell. The main player in these models is the voltage-dependent anion channel (VDAC), located in the mitochondrial outer membrane. Most metabolites including respiratory substrates, ADP, and Pi enter mitochondria only through VDAC. At the same time, high-energy phosphates are channeled out and directed to cellular energy transfer networks. Regulation of these energy fluxes is controlled by β-tubulin, bound to VDAC. It is also thought that β-tubulin‒VDAC interaction modulates cellular energy metabolism in cancer, e.g., switching from oxidative phosphorylation to glycolysis. In this review we focus on the described roles of unpolymerized αβ-tubulin heterodimers in regulating VDAC permeability for adenine nucleotides and cellular bioenergetics. We introduce the Mitochondrial Interactosome model and the function of the βII-tubulin subunit in this model in muscle cells and brain synaptosomes, and also consider the role of βIII-tubulin in cancer cells.

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Antoniou, Christos-Konstantinos, Panagiota Manolakou, Nikolaos Magkas, Konstantinos Konstantinou, Christina Chrysohoou, Polychronis Dilaveris, Konstantinos A. Gatzoulis, and Dimitrios Tousoulis. "Cardiac Resynchronisation Therapy and Cellular Bioenergetics: Effects Beyond Chamber Mechanics." European Cardiology Review 14, no. 1 (April 30, 2019): 33–44. http://dx.doi.org/10.15420/ecr.2019.2.2.

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Cardiac resynchronisation therapy is a cornerstone in the treatment of advanced dyssynchronous heart failure. However, despite its widespread clinical application, precise mechanisms through which it exerts its beneficial effects remain elusive. Several studies have pointed to a metabolic component suggesting that, both in concert with alterations in chamber mechanics and independently of them, resynchronisation reverses detrimental changes to cellular metabolism, increasing energy efficiency and metabolic reserve. These actions could partially account for the existence of responders that improve functionally but not echocardiographically. This article will attempt to summarise key components of cardiomyocyte metabolism in health and heart failure, with a focus on the dyssynchronous variant. Both chamber mechanics-related and -unrelated pathways of resynchronisation effects on bioenergetics – stemming from the ultramicroscopic level – and a possible common underlying mechanism relating mechanosensing to metabolism through the cytoskeleton will be presented. Improved insights regarding the cellular and molecular effects of resynchronisation on bioenergetics will promote our understanding of non-response, optimal device programming and lead to better patient care.

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Yang, Xingbo, Matthias Heinemann, Jonathon Howard, Greg Huber, Srividya Iyer-Biswas, Guillaume Le Treut, Michael Lynch, et al. "Physical bioenergetics: Energy fluxes, budgets, and constraints in cells." Proceedings of the National Academy of Sciences 118, no. 26 (June 17, 2021): e2026786118. http://dx.doi.org/10.1073/pnas.2026786118.

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Cells are the basic units of all living matter which harness the flow of energy to drive the processes of life. While the biochemical networks involved in energy transduction are well-characterized, the energetic costs and constraints for specific cellular processes remain largely unknown. In particular, what are the energy budgets of cells? What are the constraints and limits energy flows impose on cellular processes? Do cells operate near these limits, and if so how do energetic constraints impact cellular functions? Physics has provided many tools to study nonequilibrium systems and to define physical limits, but applying these tools to cell biology remains a challenge. Physical bioenergetics, which resides at the interface of nonequilibrium physics, energy metabolism, and cell biology, seeks to understand how much energy cells are using, how they partition this energy between different cellular processes, and the associated energetic constraints. Here we review recent advances and discuss open questions and challenges in physical bioenergetics.

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Fetterman, Jessica L., Blake R. Zelickson, Larry W. Johnson, Douglas R. Moellering, David G. Westbrook, Melissa Pompilius, Melissa J. Sammy, et al. "Mitochondrial genetic background modulates bioenergetics and susceptibility to acute cardiac volume overload." Biochemical Journal 455, no. 2 (September 27, 2013): 157–67. http://dx.doi.org/10.1042/bj20130029.

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Gyllenhammer, Lauren E., Sonja Entringer, Claudia Buss, and Pathik D. Wadhwa. "Developmental programming of mitochondrial biology: a conceptual framework and review." Proceedings of the Royal Society B: Biological Sciences 287, no. 1926 (April 29, 2020): 20192713. http://dx.doi.org/10.1098/rspb.2019.2713.

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Research on mechanisms underlying the phenomenon of developmental programming of health and disease has focused primarily on processes that are specific to cell types, organs and phenotypes of interest. However, the observation that exposure to suboptimal or adverse developmental conditions concomitantly influences a broad range of phenotypes suggests that these exposures may additionally exert effects through cellular mechanisms that are common, or shared, across these different cell and tissue types. It is in this context that we focus on cellular bioenergetics and propose that mitochondria, bioenergetic and signalling organelles, may represent a key cellular target underlying developmental programming. In this review, we discuss empirical findings in animals and humans that suggest that key structural and functional features of mitochondrial biology exhibit developmental plasticity, and are influenced by the same physiological pathways that are implicated in susceptibility for complex, common age-related disorders, and that these targets of mitochondrial developmental programming exhibit long-term temporal stability. We conclude by articulating current knowledge gaps and propose future research directions to bridge these gaps.

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Hassani, Noura, and Abdul-Kader Souid. "Perturbations in Cellular Bioenergetics: Childhood Obesity, Dyslipidemia, Diabetes and Hypoglycemia." Journal of Pediatrics and Pediatric Medicine 4, no. 1 (March 1, 2020): 1–7. http://dx.doi.org/10.29245/2578-2940/2020/1.1155.

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Paul, Bindu D., Solomon H. Snyder, and Khosrow Kashfi. "Effects of hydrogen sulfide on mitochondrial function and cellular bioenergetics." Redox Biology 38 (January 2021): 101772. http://dx.doi.org/10.1016/j.redox.2020.101772.

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Chacko, Balu, Matilda Lillian Culp, Joseph Bloomer, John Phillips, Yong-Fang Kuo, Victor Darley-Usmar, and Ashwani K. Singal. "Feasibility of cellular bioenergetics as a biomarker in porphyria patients." Molecular Genetics and Metabolism Reports 19 (June 2019): 100451. http://dx.doi.org/10.1016/j.ymgmr.2019.100451.

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