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Molecular adaptations to endurance exercise and skeletal muscle fibre plasticity
Published in Adam P. Sharples, James P. Morton, Henning Wackerhage, Molecular Exercise Physiology, 2022
The coordination of the production of mitochondrial proteins by the nucleus and mitochondrial genomes is mediated by the mitochondria transcription factors (mtTFA/TFAM and TFBM). TFAM and TFBM are encoded in nuclear DNA, translated in the cytosol and then imported into mitochondria where they activate mtDNA gene expression and mtDNA replication (Figure 9.12). The regulation of TFAM by PGC-1α was first described by work from Bruce Spiegelman’s lab. In this seminal article, Wu et al. identified PGC-1α and showed that PGC-1α increased TFAM transcription by binding to nuclear respiratory factor (NRF)1. In the wild-type promoter, PGC-1α increased TFAM transcription 4-fold. When the NRF1 binding site was mutated, PGC-1α was unable to increase TFAM and when the binding of PGC-1α and NRF1 was prevented, PGC-1α could not increase mitochondrial mass (83). These data suggest that PGC-1α drives mitochondrial transcription by co-activating NRF1 and producing more TFAM mRNA. TFAM is then translated and moves to the mitochondria and drives mtDNA replication. NRF1 can also bind to the promoters of many of the genes encoding proteins within the electron transport chain. Overexpressing NRF1 therefore results in partial mitochondrial biogenesis (84), suggesting that the increase in mitochondrial mass is regulated primarily by the co-activation of NRF1 by PGC-1α in response to exercise.
Mitochondrial Dysfunction in Chronic Disease
Published in Peter M. Tiidus, Rebecca E. K. MacPherson, Paul J. LeBlanc, Andrea R. Josse, The Routledge Handbook on Biochemistry of Exercise, 2020
Christopher Newell, Heather Leduc-Pessah, Aneal Khan, Jane Shearer
As the primary coactivator responsible for regulation of mitochondrial biogenesis, peroxisome proliferator-activated receptor-γ coactivator 1-α (PGC-1α) acts by regulating mitochondrial protein translation in response to energy balance fluctuations (23). PGC-1α is responsible for co-activating nuclear respiratory factor 2 (NRF2). Alongside NRF2, PGC-1α can then activate nuclear respiratory factor 1 (NRF1), which activates TFAM, a key activator of mitochondrial transcription within the nucleus (105) and regulator of mtDNA replication (35). Collectively, NRF1, NRF2, and TFAM ultimately enable regulation of nuclear encoded mitochondrial proteins in response to mitochondrial biogenesis, while also promoting mtDNA up-regulation to match increases in mitochondrial mass (53).
Diet and exercise interventions to promote metabolic homeostasis in TBI pathology
Published in Mark J. Ashley, David A. Hovda, Traumatic Brain Injury, 2017
TBI compromises mitochondrial bioenergetics58,59 as well as a wide range of molecular systems important for energy homeostasis, which suggests that the TBI brain is vulnerable to metabolic disorders. Several of the molecular systems closely linked to cell metabolic regulation also play important actions in the maintenance of neuronal plasticity. In particular, TBI reduces levels of the peroxisome proliferator-activated receptor gamma coactivator-1alpha (PGC-1α), which is a transcriptional regulator of various transcription factors important for maintenance of mitochondrial homeostasis.60 PGC-1α activates various transcription factors crucial for mitochondrial function, including nuclear respiratory factors (NRFs). In turn, NRFs activate the mitochondrial transcription factor A (TFAM) that regulates mitochondrial DNA (mtDNA) transcription and replication.61,62 The action of PGC-1α seems also operational for maintaining behavioral performance as these experiments have shown that latency time in the Barnes maze changes in proportion to changes in PGC-1α. The interaction between cell metabolism and neuronal plasticity is exemplified by findings that PGC-1α can also influence brain-derived neurotrophic factor (BDNF).63 Levels of BDNF are reduced after TBI, which can compromise brain plasticity and function as BDNF supports a range of metabolic events important for neuronal function.64,65 Treatment with the BDNF agonist 7,8-DHF has been shown to restore levels of PGC-1α and TFAM and mitigate TBI pathology.
Vascular endothelial growth factor alleviates mitochondrial dysfunction and suppression of mitochondrial biogenesis in models of Alzheimer’s disease
Published in International Journal of Neuroscience, 2021
Xiangtian Liu, Bingcong Chu, Suqin Jin, Maoyu Li, Yingying Xu, Hui Yang, Zhe Feng, Jianzhong Bi, Ping Wang
Mitochondrial biogenesis provides a means for maintaining healthy mitochondria, and palingenetic mitochondria from division and growth of pre-existing mitochondria. Peroxisome proliferator-activated receptor γ coactivator 1-α (PGC-1α), which interacts with two primary nuclear transcription factors (NRF), NRF1 and NRF2, represents the master regulator of mitochondrial biogenesis, [10]. NRF1 and NRF2 activate mitochondrial transcription factor A (TFAM), and TFAM then promotes nuclear encoding and mtDNA replication to activate mitochondrial biogenesis [10]. Interestingly, mitochondrial biogenesis is suppressed in AD patients, as well as in mouse and cell models of AD [10]. Although it has been shown that VEGF can induce mitochondrial biogenesis in endothelial cells [11] and adipose tissue [9], the issue of whether VEGF can restore Aβ-induced mitochondrial biogenesis suppression in AD is unknown.
Chrysanthemi Flos extract alleviated acetaminophen-induced rat liver injury via inhibiting oxidative stress and apoptosis based on network pharmacology analysis
Published in Pharmaceutical Biology, 2021
Yunfeng Zhou, Chunli Wang, Jiejian Kou, Minghui Wang, Xuli Rong, Xiaohui Pu, Xinmei Xie, Guang Han, Xiaobin Pang
The mitochondrial membrane potential is a crucial indicator of mitochondrial function, which was reduced when mitochondria are damaged. Our research presented that BZE pre-treatment increased the mitochondrial membrane potential of liver tissue in APAP-induced rats, suggesting the mitochondrial damage was mitigated by BZE. PPAR-γ and PGC-1α are key downstream targets of AMPK, taking an essential part in mitochondrial biosynthesis (Fernandes et al. 2015; Guo et al. 2018). PGC-1α can integrate and coordinate multiple transcription factors, including nuclear respiratory factor 1 (NRF1) and mitochondrial transcription factor A (TFAM). NRF1 is a transcription chaperone factor of PGC-1α, which not only regulates the transcription of nuclear genes related to the oxidative phosphorylation, but also makes effects on mitochondrial proteins encoded by mtDNA. TFAM is a nuclear-encoded protein that maintains mtDNA replication and is an important factor in mitochondrial biosynthesis (Xu et al. 2009). Our research exhibited that BZE significantly increased the levels of PPAR-γ, PGC-1α, TFAM and NRF1 in APAP-induced rat liver, indicating that BZE improved the mitochondrial function through promoting the protein expression associated to mitochondrial biosynthesis. Therefore, it is reasonable to speculate that the anti-apoptotic effect of BZE may be attributed to the improvement of mitochondrial function in APAP-induced rat liver.
Montelukast promotes mitochondrial biogenesis via CREB/PGC-1α in human bronchial epithelial cells
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2019
Huan Wang, Yali Cheng, Ying Liu, Jiang Shi, Zhe Cheng
Mitochondria are highly dynamic organelles that act as “energy factories” by generating intracellular adenosine triphosphate (ATP). Mitochondrial malfunction is important for bioenergetic metabolism and non-energetic pathological progression of various lung diseases, including bronchial asthma [1]. Mitochondrial biogenesis has been reported to be important for sustaining normal mitochondrial homeostasis in various tissue and cell types. Human bronchial epithelial mitochondria provide an essential contribution to lung diseases. Notably, increasing evidence has shown that dysregulation of mitochondrial biogenesis is linked with a diversity of lung diseases, including bronchial asthma. PGC-1α acts as a central controller of mitochondrial biogenesis [2]. In epithelial cells, activation of PGC-1α triggers the expression of NRF1 and TFAM. NRF1 drives nuclear genes to express mitochondrial proteins. TFAM is responsible for the expression of mitochondrial DNA (mtDNA) [3]. Reduced expression of PGC-1α has been linked with the pathogenesis of bronchial asthma [4]. Intervention of mitochondrial biogenesis via targeting PGC-1α has become an attractive approach for the therapy of epithelial dysfunction-associated lung diseases.