Relevant bibliographies by topics / Mitochondrial biogenesis markers

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  2. Dissertations / Theses
  3. Book chapters

Academic literature on the topic 'Mitochondrial biogenesis markers'

Author: Grafiati
Published: 3 June 2025
Last updated: 31 July 2025

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Journal articles on the topic "Mitochondrial biogenesis markers"

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Mesbah Moosavi, Zahra S., and David A. Hood. "The unfolded protein response in relation to mitochondrial biogenesis in skeletal muscle cells." American Journal of Physiology-Cell Physiology 312, no. 5 (2017): C583—C594. http://dx.doi.org/10.1152/ajpcell.00320.2016.

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Mitochondria comprise both nuclear and mitochondrially encoded proteins requiring precise stoichiometry for their integration into functional complexes. The augmented protein synthesis associated with mitochondrial biogenesis results in the accumulation of unfolded proteins, thus triggering cellular stress. As such, the unfolded protein responses emanating from the endoplasmic reticulum (UPRER) or the mitochondrion (UPRMT) are triggered to ensure correct protein handling. Whether this response is necessary for mitochondrial adaptations is unknown. Two models of mitochondrial biogenesis were us
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Jun, Lauren, Emily Knight, Tom L. Broderick, et al. "Moderate-Intensity Exercise Enhances Mitochondrial Biogenesis Markers in the Skeletal Muscle of a Mouse Model Affected by Diet-Induced Obesity." Nutrients 16, no. 12 (2024): 1836. http://dx.doi.org/10.3390/nu16121836.

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Skeletal muscle is composed of bundles of muscle fibers with distinctive characteristics. Oxidative muscle fiber types contain higher mitochondrial content, relying primarily on oxidative phosphorylation for ATP generation. Notably, as a result of obesity, or following prolonged exposure to a high-fat diet, skeletal muscle undergoes a shift in fiber type toward a glycolytic type. Mitochondria are highly dynamic organelles, constantly undergoing mitochondrial biogenesis and dynamic processes. Our study aims to explore the impact of obesity on skeletal muscle mitochondrial biogenesis and dynamic
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Zou, Peng, Longhua Liu, Louise D. Zheng, et al. "Coordinated Upregulation of Mitochondrial Biogenesis and Autophagy in Breast Cancer Cells: The Role of Dynamin Related Protein-1 and Implication for Breast Cancer Treatment." Oxidative Medicine and Cellular Longevity 2016 (2016): 1–10. http://dx.doi.org/10.1155/2016/4085727.

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Overactive mitochondrial fission was shown to promote cell transformation and tumor growth. It remains elusive how mitochondrial quality is regulated in such conditions. Here, we show that upregulation of mitochondrial fission protein, dynamin related protein-1 (Drp1), was accompanied with increased mitochondrial biogenesis markers (PGC1α, NRF1, and Tfam) in breast cancer cells. However, mitochondrial number was reduced, which was associated with lower mitochondrial oxidative capacity in breast cancer cells. This contrast might be owing to enhanced mitochondrial turnover through autophagy, bec
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Sun, Qi, Alejandro Bravo Iniguez, Qiyu Tian, Min Du та Mei-Jun Zhu. "PGC-1α Is Indispensable in Purple Potato Promoted Intestinal Epithelial Differentiation and Mitochondrial Biogenesis". Current Developments in Nutrition 6, Supplement_1 (2022): 537. http://dx.doi.org/10.1093/cdn/nzac077.040.

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Abstract Objectives Purple potato (PP) is a good dietary source of polyphenol and promotes gut epithelial health. The objective of this study is to examine the impact of PP extract on mitochondrial biogenesis and evaluate the role of peroxisome proliferator-activated receptor gamma coactivator (PGC)-1α in this. Methods In cultured colonic epithelial Caco-2 cells, the effects of PP extract on PGC-1α, cell differentiation, and markers of mitochondrial biogenesis, including mitochondrial DNA content, mitochondrial enzyme gene expression, and levels of metabolic intermediates, were first evaluated
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Jin, Sun Woo, Gi Ho Lee, Ji Yeon Kim, et al. "Effect of Porcine Whole Blood Protein Hydrolysate on Slow-Twitch Muscle Fiber Expression and Mitochondrial Biogenesis via the AMPK/SIRT1 Pathway." International Journal of Molecular Sciences 23, no. 3 (2022): 1229. http://dx.doi.org/10.3390/ijms23031229.

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Skeletal muscle is a heterogeneous tissue composed of a variety of functionally different fiber types. Slow-twitch type I muscle fibers are rich with mitochondria, and mitochondrial biogenesis promotes a shift towards more slow fibers. Leucine, a branched-chain amino acid (BCAA), regulates slow-twitch muscle fiber expression and mitochondrial function. The BCAA content is increased in porcine whole-blood protein hydrolysates (PWBPH) but the effect of PWBPH on muscle fiber type conversion is unknown. Supplementation with PWBPH (250 and 500 mg/kg for 5 weeks) increased time to exhaustion in the
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Joe, Yeonsoo, Min Zheng, Hyo Jeong Kim, et al. "Cilostazol attenuates murine hepatic ischemia and reperfusion injury via heme oxygenase-dependent activation of mitochondrial biogenesis." American Journal of Physiology-Gastrointestinal and Liver Physiology 309, no. 1 (2015): G21—G29. http://dx.doi.org/10.1152/ajpgi.00307.2014.

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Hepatic ischemia-reperfusion (I/R) can cause hepatocellular injury associated with the inflammatory response and mitochondrial dysfunction. We studied the protective effects of the phosphodiesterase inhibitor cilostazol in hepatic I/R and the roles of mitochondria and the Nrf2/heme oxygenase-1 (HO-1) system. Wild-type, Hmox1 −/−, or Nrf2 −/− mice were subjected to hepatic I/R in the absence or presence of cilostazol followed by measurements of liver injury. Primary hepatocytes were subjected to cilostazol with the HO-1 inhibitor ZnPP, or Nrf2-specific siRNA, followed by assessment of mitochond
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Tedesco, Laura, Fabio Rossi, Chiara Ruocco, et al. "Experimental evidence on the efficacy of two new metabolic modulators on mitochondrial biogenesis and function in mouse cardiomyocytes." Journal of Population Therapeutics and Clinical Pharmacology 27, SP2 (2020): e12-e21. http://dx.doi.org/10.15586/jptcp.v27isp2.740.

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Proper maintenance of mitochondrial homeostasis is essential for cell health, and mitochondrial dysfunction underlies several metabolic and heart diseases. Stimulation of mitochondrial biogenesis represents a valuable therapeutic tool for the prevention and treatment of disorders characterized by a deficit in energy metabolism. The present study aimed to potentiate the mitochondrial biogenetic efficacy of an amino acid (AA) mixture, enriched in branched-chain amino acids (BCAAs), which we previously showed to boost mitochondrial biogenesis, leading to life span extension and reducing of muscle
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Prieto-Carrasco, Rodrigo, Fernando E. García-Arroyo, Omar Emiliano Aparicio-Trejo, et al. "Progressive Reduction in Mitochondrial Mass Is Triggered by Alterations in Mitochondrial Biogenesis and Dynamics in Chronic Kidney Disease Induced by 5/6 Nephrectomy." Biology 10, no. 5 (2021): 349. http://dx.doi.org/10.3390/biology10050349.

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The five-sixth nephrectomy (5/6Nx) model is widely used to study the mechanisms involved in chronic kidney disease (CKD) progression. Mitochondrial impairment is a critical mechanism that favors CKD progression. However, until now, there are no temporal studies of the change in mitochondrial biogenesis and dynamics that allow determining the role of these processes in mitochondrial impairment and renal damage progression in the 5/6Nx model. In this work, we determined the changes in mitochondrial biogenesis and dynamics markers in remnant renal mass from days 2 to 28 after 5/6Nx. Our results s
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Wang, Yang, Zhijiang Chen, Yu Zhang, Suzhen Fang, and Qiyi Zeng. "Mitochondrial biogenesis of astrocytes is increased under experimental septic conditions." Chinese Medical Journal 127, no. 10 (2014): 1837–42. http://dx.doi.org/10.3760/cma.j.issn.0366-6999.20131934.

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Background Mitochondrial dysfunction has been reported to be one of the contributing factors of sepsis-associated encephalopathy (SAE). Mitochondrial biogenesis controls mitochondrial homeostasis and responds to changes in cellular energy demand. In addition, it is enhanced or decreased due to mitochondrial dysfunction during SAE. The aim of this study was to explore the changes of mitochondrial biogenesis of astrocytes under septic conditions. Methods Lipopolysaccharide (LPS; 50 ng/ml) and interferon-γ (IFN-γ; 200 U/ml) were incubated with astrocytes to model the effects of a septic insult on
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Sheldon, Ryan D., Grace M. Meers, E. Matthew Morris, et al. "eNOS deletion impairs mitochondrial quality control and exacerbates Western diet-induced NASH." American Journal of Physiology-Endocrinology and Metabolism 317, no. 4 (2019): E605—E616. http://dx.doi.org/10.1152/ajpendo.00096.2019.

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Dysregulated mitochondrial quality control leads to mitochondrial functional impairments that are central to the development and progression of hepatic steatosis to nonalcoholic steatohepatitis (NASH). Here, we identify hepatocellular localized endothelial nitric oxide synthase (eNOS) as a novel master regulator of mitochondrial quality control. Mice lacking eNOS were more susceptible to Western diet-induced hepatic inflammation and fibrosis in conjunction with decreased markers of mitochondrial biogenesis and turnover. The hepatocyte-specific influence was verified via magnetic activated cell
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Dissertations / Theses on the topic "Mitochondrial biogenesis markers"

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Granata, Cesare. "Effects of different exercise intensity and volume on markers of mitochondrial biogenesis in human skeletal muscle." Thesis, 2015. https://vuir.vu.edu.au/30176/.

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Mitochondria are key components of skeletal muscles as they provide the energy required for almost all cellular activities, and play an important role in ageing and cell pathology. Different forms of exercise training have been associated with mitochondrial adaptations, such as increased mitochondrial content and function, and enhanced mitochondrial biogenesis, as well as improved endurance performance. However, the role of training intensity and training volume, in determining these changes remains elusive. Therefore, the aim of this thesis was to investigate the role of training intensity an
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Book chapters on the topic "Mitochondrial biogenesis markers"

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Otth Carola, Leyton Luis, Salamin Marukel, Acuña-Hinrichsen Francisca, Martin Carolina, and Concha Margarita I. "Herpes Simplex Virus Type 1 Neuronal Infection Elicits Cellular and Molecular Mechanisms of Neuroinflammation and Neurodegeneration in in vitro and in vivo Mice Models." In Advances in Alzheimer’s Disease. IOS Press, 2017. https://doi.org/10.3233/978-1-61499-706-1-209.

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Herpes simplex virus type 1 (HSV-1) is a neurotropic virus able to establish a persistent latent infection in the host. Herpes simplex encephalitis (HSE) is associated with a high mortality rate and significant neurological, neuropsychological, and neurobehavioral sequelae, which afflict patients for life. Currently, it is unclear whether asymptomatic recurrent reactivations of HSV-1 occur in the central nervous systems in infected people, and if these events could lead to a progressive deterioration of neuronal function. In this context, HSV-1 constitutes an important candidate to be included
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Journal articles
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