Physical and Functional Cross Talk Between Endo-Sarcoplasmic Reticulum and Mitochondria in Skeletal Muscle

被引:30
作者
Boncompagni, Simona [1 ,2 ]
Pozzer, Diego [3 ]
Viscomi, Carlo [4 ]
Ferreiro, Ana [5 ,6 ]
Zito, Ester [3 ]
机构
[1] Univ G DAnnunzio, CeSI Met Ctr Res Ageing & Translat Med, Chieti, Italy
[2] Univ G DAnnunzio, DNICS, Chieti, Italy
[3] Ist Ric Farmacol Mario Negri IRCCS, Via Mario Negri 2, I-20157 Milan, Italy
[4] Univ Cambridge, MRC Mitochondrial Biol Unit, Cambridge, England
[5] Univ Paris Diderot, Unit Funct & Adapt Biol, Pathophysiol Striated Muscles Lab, Sorbonne Paris Cite,CNRS,BFA, Paris, France
[6] Grp Hosp Pitie Salpetriere, AP HP, Ctr Reference Malad Neuromusculaires Paris Est, Paris, France
基金
英国医学研究理事会;
关键词
mitochondria associated membranes; endoplasmic reticulum stress; mitochondria; congenital myopathies; calcium handling proteins; skeletal muscle; UNFOLDED PROTEIN RESPONSE; CENTRAL CORE DISEASE; ENDOPLASMIC-RETICULUM; ELECTRON-MICROSCOPY; INTRACELLULAR CA2+; INSULIN-RESISTANCE; RELEASE CHANNEL; CONTACT SITES; CALCIUM; STRESS;
D O I
10.1089/ars.2019.7934
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Recent Advances: An extensive close proximity of these two organelles is a late developmental event, which suggests that it does not have an essential function. Critical Issues: The intimate association of SR/mitochondria develops during murine postnatal differentiation and the recovery of denervated atrophic muscle, which suggests that this is a highly regulated process with a specific function. Analyses of mouse models for muscle diseases suggest that impaired ER/SR-mitochondrial contacts may be due to ER stress and lead to defective bioenergetics and insulin signaling. Future Directions: Future studies are necessary to identify the molecular determinants weakening insulin signaling upon impairment of ER/mitochondrial contacts in skeletal muscles as well as to analyze the distance between SR/ER and mitochondria in muscle diseases associated with ER stress.
引用
收藏
页码:873 / 883
页数:11
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