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Mitochondria-endoplasmic reticulum contacts in sepsis-induced myocardial dysfunction

Mitochondrial and endoplasmic reticulum (ER) are important intracellular organelles. The sites that mitochondrial and ER are closely related in structure and function are called Mitochondria-ER contacts (MERCs). MERCs are involved in a variety of biological processes, including calcium signaling, li...

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Autores principales: Jiang, Tao, Wang, Qian, Lv, Jiagao, Lin, Li
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9730255/
https://www.ncbi.nlm.nih.gov/pubmed/36506093
http://dx.doi.org/10.3389/fcell.2022.1036225
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author Jiang, Tao
Wang, Qian
Lv, Jiagao
Lin, Li
author_facet Jiang, Tao
Wang, Qian
Lv, Jiagao
Lin, Li
author_sort Jiang, Tao
collection PubMed
description Mitochondrial and endoplasmic reticulum (ER) are important intracellular organelles. The sites that mitochondrial and ER are closely related in structure and function are called Mitochondria-ER contacts (MERCs). MERCs are involved in a variety of biological processes, including calcium signaling, lipid synthesis and transport, autophagy, mitochondrial dynamics, ER stress, and inflammation. Sepsis-induced myocardial dysfunction (SIMD) is a vital organ damage caused by sepsis, which is closely associated with mitochondrial and ER dysfunction. Growing evidence strongly supports the role of MERCs in the pathogenesis of SIMD. In this review, we summarize the biological functions of MERCs and the roles of MERCs proteins in SIMD.
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spelling pubmed-97302552022-12-09 Mitochondria-endoplasmic reticulum contacts in sepsis-induced myocardial dysfunction Jiang, Tao Wang, Qian Lv, Jiagao Lin, Li Front Cell Dev Biol Cell and Developmental Biology Mitochondrial and endoplasmic reticulum (ER) are important intracellular organelles. The sites that mitochondrial and ER are closely related in structure and function are called Mitochondria-ER contacts (MERCs). MERCs are involved in a variety of biological processes, including calcium signaling, lipid synthesis and transport, autophagy, mitochondrial dynamics, ER stress, and inflammation. Sepsis-induced myocardial dysfunction (SIMD) is a vital organ damage caused by sepsis, which is closely associated with mitochondrial and ER dysfunction. Growing evidence strongly supports the role of MERCs in the pathogenesis of SIMD. In this review, we summarize the biological functions of MERCs and the roles of MERCs proteins in SIMD. Frontiers Media S.A. 2022-11-24 /pmc/articles/PMC9730255/ /pubmed/36506093 http://dx.doi.org/10.3389/fcell.2022.1036225 Text en Copyright © 2022 Jiang, Wang, Lv and Lin. https://creativecommons.org/licenses/by/4.0/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.
spellingShingle Cell and Developmental Biology
Jiang, Tao
Wang, Qian
Lv, Jiagao
Lin, Li
Mitochondria-endoplasmic reticulum contacts in sepsis-induced myocardial dysfunction
title Mitochondria-endoplasmic reticulum contacts in sepsis-induced myocardial dysfunction
title_full Mitochondria-endoplasmic reticulum contacts in sepsis-induced myocardial dysfunction
title_fullStr Mitochondria-endoplasmic reticulum contacts in sepsis-induced myocardial dysfunction
title_full_unstemmed Mitochondria-endoplasmic reticulum contacts in sepsis-induced myocardial dysfunction
title_short Mitochondria-endoplasmic reticulum contacts in sepsis-induced myocardial dysfunction
title_sort mitochondria-endoplasmic reticulum contacts in sepsis-induced myocardial dysfunction
topic Cell and Developmental Biology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9730255/
https://www.ncbi.nlm.nih.gov/pubmed/36506093
http://dx.doi.org/10.3389/fcell.2022.1036225
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