Emerging role of mitophagy in myoblast differentiation and skeletal muscle remodeling

被引:11
作者
Rahman, F. Ahmad [1 ]
Quadrilatero, Joe [1 ,2 ]
机构
[1] Univ Waterloo, Dept Kinesiol & Hlth Sci, Waterloo, ON, Canada
[2] Univ Waterloo, Fac Hlth, 200 Univ Ave West, Waterloo, ON N2L 3G1, Canada
基金
加拿大自然科学与工程研究理事会;
关键词
Mitophagy; Autophagy; Mitochondria; Mitochondrial network; Skeletal muscle; Myoblasts; Fiber type; Remodeling; Differentiation; Myogenesis; Regeneration; Atrophy; Aging; Cancer; CELL-DEATH; MITOCHONDRIAL DYNAMICS; INDUCED AUTOPHAGY; OXIDATIVE STRESS; SATELLITE CELLS; QUALITY-CONTROL; BNIP3; PROTEIN; PINK1; APOPTOSIS; EXERCISE;
D O I
10.1016/j.semcdb.2021.11.026
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Mitochondrial turnover in the form of mitophagy is emerging as a central process in maintaining cellular function. The degradation of damaged mitochondria through mitophagy is particularly important in cells/tissues that exhibit high energy demands. Skeletal muscle is one such tissue that requires precise turnover of mito-chondria in several conditions in order to optimize energy production and prevent bioenergetic crisis. For instance, the formation of skeletal muscle (i.e., myogenesis) is accompanied by robust turnover of low -functioning mitochondria to eventually allow the formation of high-functioning mitochondria. In mature skel-etal muscle, alterations in mitophagy-related signaling occur during exercise, aging, and various disease states. Nonetheless, several questions regarding the direct role of mitophagy in various skeletal muscle conditions remain unknown. Furthermore, given the heterogenous nature of skeletal muscle with respect to various cellular and molecular properties, and the plasticity in these properties in various conditions, the involvement and characterization of mitophagy requires more careful consideration in this tissue. Therefore, this review will highlight the known mechanisms of mitophagy in skeletal muscle, and discuss their involvement during myo-genesis and various skeletal muscle conditions. This review also provides important considerations for the ac-curate measurement of mitophagy and interpretation of data in skeletal muscle.
引用
收藏
页码:54 / 65
页数:12
相关论文
共 162 条
[51]   Exercise-Induced Mitophagy in Skeletal Muscle and Heart [J].
Guan, Yuntian ;
Drake, Joshua C. ;
Yan, Zhen .
EXERCISE AND SPORT SCIENCES REVIEWS, 2019, 47 (03) :151-156
[52]   Sex-Based Differences in Skeletal Muscle Kinetics and Fiber-Type Composition [J].
Haizlip, K. M. ;
Harrison, B. C. ;
Leinwand, L. A. .
PHYSIOLOGY, 2015, 30 (01) :30-39
[53]   Microtubule-associated Protein 1 Light Chain 3 (LC3) Interacts with Bnip3 Protein to Selectively Remove Endoplasmic Reticulum and Mitochondria via Autophagy [J].
Hanna, Rita A. ;
Quinsay, Melissa N. ;
Orogo, Amabel M. ;
Giang, Kayla ;
Rikka, Shivaji ;
Gustafsson, Asa B. .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2012, 287 (23) :19094-19104
[54]   Myogenic satellite cells: physiology to molecular biology [J].
Hawke, TJ ;
Garry, DJ .
JOURNAL OF APPLIED PHYSIOLOGY, 2001, 91 (02) :534-551
[55]  
He Y. -L., 2020, BIORXIV, DOI [10.1101/2020.08.27.271270,2020.08.27.271270, DOI 10.1101/2020.08.27.271270,2020.08.27.271270]
[56]   The PINK1-PARKIN Mitochondrial Ubiquitylation Pathway Drives a Program of OPTN/NDP52 Recruitment and TBK1 Activation to Promote Mitophagy [J].
Heo, Jin-Mi ;
Ordureau, Alban ;
Paulo, Joao A. ;
Rinehart, Jesse ;
Harper, J. Wade .
MOLECULAR CELL, 2015, 60 (01) :7-20
[57]   MitoTimer A novel tool for monitoring mitochondrial turnover [J].
Hernandez, Genaro ;
Thornton, Christine ;
Stotland, Aleksandr ;
Lui, Diana ;
Sin, Jon ;
Ramil, Jennifer ;
Magee, Najib ;
Andres, Allen ;
Quarato, Giovanni ;
Carreira, Raquel S. ;
Sayen, M. Richard ;
Wolkowicz, Roland ;
Gottlieb, Roberta A. .
AUTOPHAGY, 2013, 9 (11) :1852-1861
[58]   Transcriptional regulation of BNIP3 by Sp3 in prostate cancer [J].
Huang, Ying ;
Shen, Pengfei ;
Chen, Xueqin ;
Chen, Zhibin ;
Zhao, Tao ;
Chen, Ni ;
Gong, Jing ;
Nie, Ling ;
Xu, Miao ;
Li, Xinglan ;
Zeng, Hao ;
Zhou, Qiao .
PROSTATE, 2015, 75 (14) :1556-1567
[59]   Parkin-catalyzed Ubiquitin-Ester Transfer Is Triggered by PINK1-dependent Phosphorylation [J].
Iguchi, Masahiro ;
Kujuro, Yuki ;
Okatsu, Kei ;
Koyano, Fumika ;
Kosako, Hidetaka ;
Kimura, Mayumi ;
Suzuki, Norihiro ;
Uchiyama, Shinichiro ;
Tanaka, Keiji ;
Matsuda, Noriyuki .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2013, 288 (30) :22019-22032
[60]   Bcl-2/E1B 19kDa-interacting protein 3-like protein (Bnip3L) interacts with Bcl-2/Bcl-xL and induces apoptosis by altering mitochondrial membrane permeability [J].
Imazu, T ;
Shimizu, S ;
Tagami, S ;
Matsushima, M ;
Nakamura, Y ;
Miki, T ;
Okuyama, A ;
Tsujimoto, Y .
ONCOGENE, 1999, 18 (32) :4523-4529