A link between protein acetylation and mitochondrial dynamics under energy metabolism: A comprehensive overview

Abstract

Cells adjust mitochondrial morphologies to coordinate between the cellular demand for energy and the availability of resources. Mitochondrial morphology is regulated by the balance between two counteracting mitochondrial processes of fusion and fission. Fission and fusion are dynamic and reversible processes that depend on the coordination of a number of proteins and are primarily regulated by posttranslational modifications. In the mitochondria, more than 20% of proteins are acetylated in proteomic surveys, partly involved in the dynamic regulation of mitochondrial fusion and fission. This article focuses on the molecular mechanism of the mitochondrial dynamics of fusion and fission, and summarizes the related mechanisms and targets of mitochondrial protein acetylation to regulate the mitochondrial dynamics of fusion and fission in energy metabolism.

PDHA1 hyperacetylation-mediated lactate overproduction promotes sepsis-induced acute kidney injury via Fis1 lactylation

“…Given that mitochondrial dysfunction is an important pathogenesis of SAKI and acetylation plays a pivotal role in regulating mitochondrial protein function [ 26 – 28 ], a Tandem Mass Tags (TMT)-labeled acetylome was used to identify changes in the acetylation of renal mitochondrial proteins 8 h after cecal ligation and puncture (CLP) in C57BL/6 mice (Fig. 1A ).…”

Cardioprotective Action of a Novel Synthetic 19,20-EDP Analog Is Sirt Dependent

“…Sirtuins are a family of NAD + -dependent deacetylase enzymes, consisting of 7 members, which can regulate a vast array of mitochondrial proteins through deacetylation activity, including many involved in respiration, oxidative stress responses, metabolism, and mitochondrial dynamics. [18][19][20] The relative pH and abundance of acetyl-CoA contribute to greater than 65% of mitochondrial proteins being acetylated under normal physiological conditions. The mitochondrial antioxidant ROS-scavenger MnSOD 2 has its activity significantly upregulated on deacetylation by SIRT3.…”

“…18 Owing to high pH, most mitochondrial proteins are acetylated under physiological conditions and as such can be activated by SIRT3. 19,20 Subsequently, SIRT3 has been shown to be involved in mitochondrial biology, from dynamic fission/fusion and respiration to antioxidant processes, and is critical for adaptive cellular responses to various stresses, such as ischemia. 15,18,21,22 Growing evidence indicates that pyroptosis plays a central role in the pathogenesis of myocardial IR injury, where enhanced sirtuin activity can blunt the response.…”