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Preserved in Portico This version is not peer-reviewed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
Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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