User:Napmier/MOTS-c
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MOTS-c
[edit]MOTS-c (mitochondrial open reading frame of the 12S rRNA-c) is a peptide encoded in mitochondrial DNA. MOTS-c was discovered in 2015 through an analysis of the human 12S rRNA region as researchers were looking for short open reading frames (sORFs). [1] MOTS-c was found in the mitochondria, the organelle responsible for metabolism and energy conversion. Mitochondrial-derived peptides (MDPs) make up mitochondrial DNA genes, which are translated from sORFs. Today only eight different types of MDPs have been identified. The discovery of MOTS-c has led to many new areas of research as each MDP has its own role in causing different biological response. For MOTS-c's case, it affects aging disorders, muscle fiber strength, bone formation, inflammatory responses, and exercising factors. Understanding MOTS-c's role in the body could pave the way for new treatment options targeting its previously discussed functions. [2]
Physiological Effects
[edit]Aging
[edit]As individuals get older, there is a progressive decline in metabolic activity alongside worsening of physical function. As this peptide is encoded in the mitochondrial DNA, it plays a crucial role in regulation of metabolism and maintenance of the mitochondrial homeostasis. It has been speculated that this peptide promotes enhancement of physical performance in all ages of mice.[3] The specific mechanism in how exercise regulates the expression of MOTS-c is not well researched.
Specifically in skeletal muscle and plasma among healthy males, research suggests that the age-related shift from fast- to slow-twitch muscle fibers may play a role in the elevated muscle MOTS-c levels. Furthermore, this change could be associated with the diminished correlation between the usual plasma-to-muscle MOTS-c ratio in older adults.[4]
Alongside the degradation of metabolic function and muscle fibers, the breakdown of bone also occurs during the aging process. As you age, the balance of bone remodeling shifts, leading to accelerated bone loss, particularly in key supportive structures of the body. MOTS-c treatment was found to alleviate this bone loss by inhibiting the bone resorption through osteoclasts thus stimulating the proliferation of osteoblast. These effects contributed by MOTS-c may be helpful in osteoclast related disease due to the pathway that it induces.[5][2]
Immune System
[edit]Overproduction of inflammatory factors, which result in overreaction of response, could lead to disfunction and damage in internal tissues. MOTS-c has been shown to reduce pro-inflammatory cytokines and increase auto-inflammatory factors and insulin stimulated glucose treatments which can impact glucose homeostasis.[1] These anti-inflammatory effects of MOTS-c are largely mediated through the activation of AMP-activated protein kinases (AMPK) pathway, which is a key regulator of cellular metabolism and inflammation. As it reduces pro-inflammatory cytokines, it promotes anti-inflammatory cytokines like IL-10. [6] Research is still being done to investigate if this could be used as a therapeutic agent for inflammatory diseases like arthritis, metabolic disorders and certain types of cancers.[2]
Exercise
[edit]MOTS-c plays a crucial role in cardiovascular health by protecting cardiomyocytes and by enhancing endothelial function.[7] This conclusion was made through a mouse study that looked into the cardiac improvements in exercised rats with and without MOTS-c treatment, the finding told the researchers based on the significant findings, MOTS-c could modulate the cardiovascular benefits of training.[2]
Another mouse study, looked at the the correlation between respiratory exchanged and glucose utilization. It was found that over three weeks the group of mice fed a high-fat diet, administration of MOTS-c resulted in an increase of respiratory exchange ratio implying that MOTS-c enhanced glucose utilization. This group of mice exhibited a significantly higher heat production indicating that it increased the energy expenditure. These changes occurred without a change of lifestyle of the rats implying that MOTS-c can be used to prevent high fat diet induced obesity by boosting the energy production and improving glucose metabolism.[3]
References
[edit]- ^ a b Lee, Changhan; Zeng, Jennifer; Drew, Brian; Sallam, Tamer; Martin-Montalvo, Alejandro; Wan, Junxiang; Kim, Su-Jeong; Mehta, Hemal; Hevener, Andrea; Cabo, Rafael; Cohen, Pinchas (March 3, 2016). "The Mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance". National Library of Medicine.
- ^ a b c d Zheng, Yuejun; Wei, Zilin; Wang, Tianhui (January 25, 2023). "MOTS-c: A promising mitochondrial-derived peptide for therapeutic exploitation". MOTS-c: A promising mitochondrial-derived peptide for therapeutic exploitation.
- ^ a b Reynolds, Joseph; Lai, Rochelle; Woodhead, Jonathan; Joly, James; Mitchell, Cameron; Cameron-Smith, Cameron; Lu, Ryan; Cohen, Pinchas; Graham, Nicholas; Benayoun, Bérénice; Merry, Troy; Lee, Changhan. "MOTS-c is an exercise-induced mitochondrial-encoded regulator of age-dependent physical decline and muscle homeostasis". National Library of Medicine.
- ^ D'Souza, Randall; Woodhead, Jonathan; Hedges, Christopher; Zeng, Nina; Wan, Junxiang; Kumagai, Hiroshi; Lee, Changhan; Cohen, Pinchas; Cameron-Smith, David; Mitchell, Cameron; Merry, Troy. "Increased expression of the mitochondrial derived peptide, MOTS-c, in skeletal muscle of healthy aging men is associated with myofiber composition". National Library of Medicine.
- ^ Ming, Wei; Lu, Gan; Xin, Sha; Huanyu, Lu; Yinghao, Jiang; Xiaoying, Lei; Chengming, Xu; Banjun, Ruan; Li, Wang; Zifan, Lu. "Mitochondria related peptide MOTS-c suppresses ovariectomy-induced bone loss via AMPK activation". Science Direct.
- ^ Wen, Wei; Zhang, Lieliang; Lin, Yue; Rao, Xiuqing; Hua, Fuzhou; Ying, Jun (January 20, 2023). "Mitochondria-derived peptide MOTS-c: effects and mechanisms related to stress, metabolism and aging". National Library of Medicine.
- ^ Yuan, Jinghan; Wang, Manda; Pan, Yanrong; Liang, Min; Fu, Yu; Duan, Yimei; Tang, Mi; Laher, Ismail; Li, Shuchang. "The mitochondrial signaling peptide MOTS-c improves myocardial performance during exercise training in rats". Scientific Reports Nature.