Preprint Review Version 1 Preserved in Portico This version is not peer-reviewed

Calpain and Cardiometabolic Diseases

Version 1 : Received: 13 October 2023 / Approved: 13 October 2023 / Online: 17 October 2023 (03:30:33 CEST)

A peer-reviewed article of this Preprint also exists.

Miyazaki, T. Calpain and Cardiometabolic Diseases. Int. J. Mol. Sci. 2023, 24, 16782. Miyazaki, T. Calpain and Cardiometabolic Diseases. Int. J. Mol. Sci. 2023, 24, 16782.

Abstract

Calpain is delineated as a superfamily of cysteine proteases containing a CysPC motif within their genes. Among the fifteen species of mammalian homologs, calpain-1 and -2, which are categorized as conventional isozymes, execute limited proteolysis in a calcium-dependent fashion. Accordingly, the calpain system participates in physiological and pathological phenomena, encompassing cell migration, apoptosis, skeletal muscle integrity, and synaptic plasticity. The dysregulation of the calpain system has been inextricably linked to a multitude of diseases, such as ischemic and degenerative diseases, rendering it a subject of profound interest in the fields of basic research and pharmaceutical development aimed at therapeutic interventions. Recent investigations have unveiled the contributions of both conventional and unconventional calpains to the pathogenesis of cardiometabolic disorders, such as atherosclerosis, diabetes, and hepatic diseases. Consequently, the present review accentuates the pivotal role of calpains in the complications of cardiometabolic diseases and embarks upon a discourse regarding calpains as molecular targets.

Keywords

alternative mRNA splicing; amino acids; inflammation; dyslipidemia; macrophages; NAFLD; NASH; regulatory T cells; vascular endothelial cells

Subject

Medicine and Pharmacology, Pathology and Pathobiology

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