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Exercise-Induced Mitochondrial Biogenesis: Molecular Regulation, Impact of Training, and Influence on Exercise Performance
Published in Peter M. Tiidus, Rebecca E. K. MacPherson, Paul J. LeBlanc, Andrea R. Josse, The Routledge Handbook on Biochemistry of Exercise, 2020
Hashim Islam, Jacob T. Bonafiglia, Cesare Granata, Brendon J. Gurd
The final steps leading to mitochondrial biogenesis involve the targeting of cytosolic precursor protein to the mitochondria and their subsequent import and redistribution to their final destination within the organelle (51, 52). Given the nuclear origin of the vast majority of mitochondrial proteins, these terminal steps are particularly important for ensuring that earlier adaptive events (e.g., signalling, gene transcription, protein synthesis) are successfully converted into alterations in mitochondrial phenotype. In this regard, cytosolic chaperones unfold and direct precursor protein to specific compartments within the organelle based on the presence of a cleavable target sequence (51, 52). The transport of mitochondrial-destined protein is accomplished by translocase complexes of the outer and (for matrix-destined protein) inner membranes (TOM and TIM, respectively) (51, 52). Upon its arrival to the appropriate mitochondrial sub-compartment (e.g., matrix), the target sequence is removed from the precursor protein, which is subsequently refolded and directed to its final destination by mitochondrial chaperones, leading to the expansion of the mitochondrial reticulum (51, 52).
Mitochondrial Mechanisms of Tubular Injury
Published in Robin S. Goldstein, Mechanisms of Injury in Renal Disease and Toxicity, 2020
Rick G. Schnellmann, Richard D. Griner
In addition to these indirect probings, direct measurements of enzyme activity is a common technique to assess impairment of the tricarboxylic acid cycle enzymes or to the F0F1-ATPase. Inhibitors of specific mitochondrial functions such as atractyloside, to inhibit ADP/ATP translocase, and oligomycin are frequently used during measurements of ATPase activity and QO2. Conversely, more qualitative determinations such as morphological examinations are typically made to reveal gross changes in mitochondrial structure. Finally, the consequence of mitochondrial dysfunction, decreases in cellular ATP, and other adenine nucelotides can be determined by a variety of methods.
Phospholipids and the Clotting Process
Published in E. Nigel Harris, Thomas Exner, Graham R. V. Hughes, Ronald A. Asherson, Phospholipid-Binding Antibodies, 2020
Robert F. A. Zwaal, Edouard M. Bevers, Jan Rosing
Recently, an entirely different mechanism has been proposed to regulate asymmetric phospholipid distributions in biological membranes. When exogenous amino-phospholipids are introduced into the external leaflet of red cell membranes, they are rapidly translocated to the inner leaflet,107-110 with half-times of 5 min and 1 h at 37°C for phosphatidylserine and phosphatidylethanolamine, respectively. Meanwhile, this phenomenon has been observed in a variety of other cells,110 including platelets.123 The process is ATP-dependent and selective for amino-phospholipids compared to choline-phospholipids. Moreover, outward-inward translocase activity is inhibited by intracellular calcium, sulfhydryl reactive reagents and D-isomers of phosphatidylserine and phosphatidylethanolamine.124,125 Interestingly, Connor and Schroit124 have shown that inhibition of translocase activity following sulfhydryl oxidation can be undone after reducing the membrane with dithiothreitol.
Passive heat stress induces mitochondrial adaptations in skeletal muscle
Published in International Journal of Hyperthermia, 2023
Erik D. Marchant, W. Bradley Nelson, Robert D. Hyldahl, Jayson R. Gifford, Chad R. Hancock
Aside from the apparent role of HSP72 in activating PGC-1α through AMPK and SIRT1, heat shock proteins play a vital role in the import of nuclear-encoded mitochondrial proteins into the mitochondrial matrix, as well as in helping fold and assemble them into complexes [52]. The mitochondrial proteome is composed of over 1,000 proteins, 99% of which are nuclear encoded, with only 13 being coded for by mitochondrial DNA [80]. Because most mitochondrial proteins are translated outside the mitochondria, specialized import machinery is required to introduce newly synthesized proteins into the mitochondrial matrix. Two primary players in this process are the translocase of the outer membrane (TOM), and the translocase of the inner membrane (TIM) [81]. Interestingly, both cytosolic and mitochondrial heat shock proteins are vital for this translocation process, partially due to their interactions with TIM and TOM [81–83]. Furthermore, once introduced into the mitochondria, heat shock protein 60 is necessary for the proper folding and assembly of the respiratory complexes of the electron transport system [84]. To date, it is unknown if passive heating in humans or animals improves protein import and folding due to increased HSP content or activation in skeletal muscle. However, the vital role of HSPs in mitochondrial protein import and assembly suggests that this is an important area for future research.
Omentin-1 promotes mitochondrial biogenesis via PGC1α-AMPK pathway in chondrocytes
Published in Archives of Physiology and Biochemistry, 2023
Zhigang Li, Yao Zhang, Fengde Tian, Zihua Wang, Haiyang Song, Haojie Chen, Baolin Wu
The mitochondrion is the "powerhouse" in eukaryotic cells. Mitochondrial biogenesis is the process of increasing cellular metabolic capacity, featured with the synthesis of enzymes for both glycolysis and oxidative phosphorylation (Jornayvaz and Shulman 2010). An efficient mitochondrial biogenesis needs the import of nuclear protein as well as mitochondrial replication, mitochondrial fusion and fission (Nunnari and Suomalainen 2012). Mitochondria in mammalian cells contain more than 1500 proteins, but only 13 proteins are coded in mitochondrial DNA, a majority of them are synthesised from nuclear DNA coding genes. Various mitochondrial molecular markers are used to study the mitochondrial regulation in eukaryotes. Translocase of the outer membrane (TOM) complex is a membrane-bound translocator vital to import mitochondrial precursors, and TOM complex includes several subunits including TOM20, TOM40 and TOM70 and is secured by TOM5, TOM6, TOM7, etc. (Ahting et al.1999). Several subunits of mitochondrial ATP synthases are also used as the markers of functional mitochondria, including ATPA, ATP5C1, ATPD and other subunits. The electron transport chain (ETC) located within the mitochondrial inner membrane composes of four protein complexes. Succinate dehydrogenase complex iron-sulfur subunit B (SDHB) links the pathways of Krebs cycle and oxidative phosphorylation. Mitochondrial DNA encoded subunits (MTCO1, MTCO2, MTCO3) are important subunits of complex IV (Zhao et al.2019).
Qushi Huayu decoction attenuated hepatic lipid accumulation via JAK2/STAT3/CPT-1A-related fatty acid β-oxidation in mice with non-alcoholic steatohepatitis
Published in Pharmaceutical Biology, 2022
QinMei Sun, Xin Wang, Xin Xin, ZiMing An, YiYang Hu, Qin Feng
Mitochondrial fatty acid β-oxidation (FAO) is the primary mechanism responsible for fat consumption. Free fatty acids (FFAs) are esterified with coenzyme A, transported to the mitochondrial matrix, and oxidized to produce acetyl coenzyme A, which eventually undergoes β-oxidation (Dai et al. 2018). In FAO, carnitine palmitoyl transferase (CPT) systems mediate the transport of FFAs. These systems consist of three proteins: CPT-1, CPT-2 and acylcarnitine translocase. CPT-1, which is the rate-limiting enzyme of FAO, is responsible for the initial enzymatic reaction for FFA transport. Activation of CPT-1 promotes energy expenditure and has metabolic benefits (Shin et al. 2006). It is well known that mitochondrial dysfunction contributes to the onset of NAFLD because it affects liver lipid homeostasis and promotes lipid peroxidation, cytokine release and cell death (Begriche et al. 2006). Increasing evidence suggests that improving mitochondrial dysfunction is an effective strategy for reducing lipid overload. In conclusion, there is evidence that promoting FAO for the condition of hepatic fat accumulation has significant benefits.