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      Compositions and Functions of Mitochondria-Associated Endoplasmic Reticulum Membranes and Their Contribution to Cardioprotection by Exercise Preconditioning

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          Abstract

          Mitochondria-associated endoplasmic reticulum membranes (MAMs) are important components of intracellular signaling and contribute to the regulation of intracellular Ca 2+/lipid homeostasis, mitochondrial dynamics, autophagy/mitophagy, apoptosis, and inflammation. Multiple studies have shown that proteins located on MAMs mediate cardioprotection. Exercise preconditioning (EP) has been shown to protect the myocardium from adverse stimuli, but these mechanisms are still being explored. Recently, a growing body of evidence points to MAMs, suggesting that exercise or EP may be involved in cardioprotection by modulating proteins on MAMs and subsequently affecting MAMs. In this review, we summarize the latest findings on MAMs, analyzing the structure and function of MAMs and the role of MAM-related proteins in cardioprotection. We focused on the possible mechanisms by which exercise or EP can modulate the involvement of MAMs in cardioprotection. We found that EP may affect MAMs by regulating changes in MFN2, MFN1, AMPK, FUNDC1, BECN1, VDAC1, GRP75, IP3R, CYPD, GSK3β, AKT, NLRP3, GRP78, and LC3, thus playing a cardioprotective role. We also provided direction for future studies that may be of interest so that more in-depth studies can be conducted to elucidate the relationship between EP and cardioprotection.

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          Most cited references144

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          Myocardial reperfusion injury.

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            An ER-mitochondria tethering complex revealed by a synthetic biology screen.

            Communication between organelles is an important feature of all eukaryotic cells. To uncover components involved in mitochondria/endoplasmic reticulum (ER) junctions, we screened for mutants that could be complemented by a synthetic protein designed to artificially tether the two organelles. We identified the Mmm1/Mdm10/Mdm12/Mdm34 complex as a molecular tether between ER and mitochondria. The tethering complex was composed of proteins resident of both ER and mitochondria. With the use of genome-wide mapping of genetic interactions, we showed that the components of the tethering complex were functionally connected to phospholipid biosynthesis and calcium-signaling genes. In mutant cells, phospholipid biosynthesis was impaired. The tethering complex localized to discrete foci, suggesting that discrete sites of close apposition between ER and mitochondria facilitate interorganelle calcium and phospholipid exchange.
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              Preconditioning with ischemia: a delay of lethal cell injury in ischemic myocardium.

              Circulation, 74(5), 1124-1136
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                Author and article information

                Contributors
                Journal
                Front Physiol
                Front Physiol
                Front. Physiol.
                Frontiers in Physiology
                Frontiers Media S.A.
                1664-042X
                06 June 2022
                2022
                : 13
                : 910452
                Affiliations
                College of Physical Education and Health , Guangxi Normal University , Guilin, China
                Author notes

                Edited by: Pasquale Vergara, San Raffaele Hospital (IRCCS), Italy

                Reviewed by: Allen Mariano Andres, Arima Genomics, United States

                Dhanendra Tomar, Wake Forest School of Medicine, United States

                *Correspondence: Fenglin Peng, pengflin@ 123456mailbox.gxnu.edu.cn

                This article was submitted to Exercise Physiology, a section of the journal Frontiers in Physiology

                Article
                910452
                10.3389/fphys.2022.910452
                9207531
                35733995
                6fa60a18-f547-485a-8fe0-5de1259059bf
                Copyright © 2022 Lv, Cheng and Peng.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 01 April 2022
                : 11 May 2022
                Categories
                Physiology
                Review

                Anatomy & Physiology
                mitochondria-associated endoplasmic reticulum membranes,exercise preconditioning,cardioprotection,exercise,preconditioning,heart

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