Mitochondria-endoplasmic reticulum contacts in sepsis-induced myocardial dysfunction

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.

FIGURE 1

Key cellular functions and proteins involved in MERCs. (A) Calcium signaling. (B) Lipid synthesis and transport. (C) Autophagy. (D) Mitochondrial dynamics. (E) ER stress and inflammtion. Figures were created using Figdraw. ER, endoplasmic reticulum; MERCs, mitochondria-endoplasmic reticulum contacts.

FIGURE 2

MERCs as potential new therapeutic targets for treatment of SIMD. MERCs regulates some important biological functions, including calcium signaling, autophagy, mitochondrial dynamics, ER stress, and inflammation. The abnormality of these processes often leads to SIMD. Notably, the key regulatory proteins of these processes can serve as potential therapeutic targets for SIMD. Figures were created using Figdraw. ER, endoplasmic reticulum; MERCs, mitochondria-endoplasmic reticulum contacts; SIMD, sepsis-induced myocardial dysfunction.