Mitochondria-endoplasmic reticulum contacts in sepsis-induced myocardial dysfunction

Tao Jiang; Qian Wang; Jiagao Lv; Li Lin

doi:10.3389/fcell.2022.1036225

Mitochondria-endoplasmic reticulum contacts in sepsis-induced myocardial dysfunction

Front Cell Dev Biol. 2022 Nov 24:10:1036225. doi: 10.3389/fcell.2022.1036225. eCollection 2022.

Authors

Tao Jiang^{1

2}, Qian Wang², Jiagao Lv², Li Lin²

Affiliations

¹ Department of Geriatrics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
² Division of Cardiology, Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Abstract

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.

Keywords: ER stress; autophagy; calcium signaling; inflammation; mitochondria-ER contacts; mitochondrial dynamics; sepsis-induced myocardial dysfunction.

Publication types

Review