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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, et al. "Integration of cellular bioenergetics with mitochondrial quality control and autophagy." Biological Chemistry 393, no. 12 (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

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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 (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 extrace

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3

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 (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 = 6

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4

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

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5

Acuña-Castroviejo, Darío, Miguel Martín, Manuel Macías, et al. "Melatonin, mitochondria, and cellular bioenergetics." Journal of Pineal Research 30, no. 2 (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 (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

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7

Davies, Karen M., and Bertram Daum. "Role of cryo-ET in membrane bioenergetics research." Biochemical Society Transactions 41, no. 5 (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 ha

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8

Chacko, Balu K., Philip A. Kramer, Saranya Ravi, et al. "The Bioenergetic Health Index: a new concept in mitochondrial translational research." Clinical Science 127, no. 6 (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 pr

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9

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

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10

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 (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

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11

Gevezova, Maria, Danail Minchev, Iliana Pacheva, et al. "Cellular Bioenergetic and Metabolic Changes in Patients with Autism Spectrum Disorder." Current Topics in Medicinal Chemistry 21, no. 11 (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.

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12

Liu, Haoming, Yingying Du, Jean-Philippe St-Pierre, et al. "Bioenergetic-active materials enhance tissue regeneration by modulating cellular metabolic state." Science Advances 6, no. 13 (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 o

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13

Padhi, Abinash, Alexander H. Thomson, Justin B. Perry, et al. "Bioenergetics underlying single-cell migration on aligned nanofiber scaffolds." American Journal of Physiology-Cell Physiology 318, no. 3 (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 us

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14

Riddle, Ryan C., and Thomas L. Clemens. "Bone Cell Bioenergetics and Skeletal Energy Homeostasis." Physiological Reviews 97, no. 2 (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

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15

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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16

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

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17

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

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18

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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19

Mishra, Jay S., Chellakkan S. Blesson, and Sathish Kumar. "Testosterone Decreases Placental Mitochondrial Content and Cellular Bioenergetics." Biology 9, no. 7 (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 o

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20

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 (2017): S1112. http://dx.doi.org/10.1016/s0016-5085(17)33747-2.

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21

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

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22

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 (2010): 465–82. http://dx.doi.org/10.1038/nrd3138.

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23

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

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24

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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25

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 (2012): 1740–46. http://dx.doi.org/10.1016/j.bbabio.2012.02.028.

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26

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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27

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

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28

Serbulea, Vlad, Clint M. Upchurch, Michael S. Schappe, et al. "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 (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 a

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29

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 (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 ma

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30

Mishra, Prashant, and David C. Chan. "Metabolic regulation of mitochondrial dynamics." Journal of Cell Biology 212, no. 4 (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 em

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31

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

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32

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

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33

Shangguan, Fugen, Yan Liu, Li Ma, et al. "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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34

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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35

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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36

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

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37

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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38

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

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39

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 (2011): 46a. http://dx.doi.org/10.1016/j.bpj.2010.12.450.

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40

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

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41

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 (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

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42

Wright, JaLessa N., Gloria A. Benavides, Michelle S. Johnson, et al. "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 (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 acut

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43

Puurand, Marju, Kersti Tepp, Natalja Timohhina та ін. "Tubulin βII and βIII Isoforms as the Regulators of VDAC Channel Permeability in Health and Disease". Cells 8, № 3 (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 in

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44

Antoniou, Christos-Konstantinos, Panagiota Manolakou, Nikolaos Magkas, et al. "Cardiac Resynchronisation Therapy and Cellular Bioenergetics: Effects Beyond Chamber Mechanics." European Cardiology Review 14, no. 1 (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 impr

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45

Yang, Xingbo, Matthias Heinemann, Jonathon Howard, et al. "Physical bioenergetics: Energy fluxes, budgets, and constraints in cells." Proceedings of the National Academy of Sciences 118, no. 26 (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 defi

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46

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

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47

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 (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,

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48

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 (2020): 1–7. http://dx.doi.org/10.29245/2578-2940/2020/1.1155.

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49

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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50

Chacko, Balu, Matilda Lillian Culp, Joseph Bloomer, et al. "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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