Tale of two kinases:Protein kinase A and Ca^(2+)/calmodulin-dependent protein kinase Ⅱ in pre-diabetic cardiomyopathy  

作　　者：Pamela Gaitán-González Rommel Sánchez-Hernández José-Antonio Arias-Montaño Angélica Rueda 

机构地区：[1]Department of Biochemistry,Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional,Ciudad de México 07360,Mexico [2]Department of Physiology,Biophysics and Neurosciences,Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional,Ciudad de México 07360,Mexico

出　　处：《World Journal of Diabetes》2021年第10期1704-1718,共15页世界糖尿病杂志（英文版）（电子版）

基　　金：Supported by SEP-Cinvestav Project,No.FIDSC 2018/2;and SEP-Conacyt Ciencia Básica 2017-2018,No.A1-S-9082(to Rueda A).

摘　　要：Metabolic syndrome is a pre-diabetic state characterized by several biochemical and physiological alterations,including insulin resistance,visceral fat accumulation,and dyslipidemias,which increase the risk for developing cardiovascular disease.Metabolic syndrome is associated with augmented sympathetic tone,which could account for the etiology of pre-diabetic cardiomyopathy.This review summarizes the current knowledge of the pathophysiological consequences of enhanced and sustainedβ-adrenergic response in pre-diabetes,focusing on cardiac dysfunction reported in diet-induced experimental models of pre-diabetic cardiomyopathy.The research reviewed indicates that both protein kinase A and Ca^(2+)/calmodulin-dependent protein kinase Ⅱ play important roles in functional responses mediated byβ1-adrenoceptors;therefore,alterations in the expression or function of these kinases can be deleterious.This review also outlines recent information on the role of protein kinase A and Ca^(2+)/calmodulin-dependent protein kinase Ⅱ in abnormal Ca^(2+)handling by cardiomyocytes from diet-induced models of pre-diabetic cardiomyopathy.

关 键 词：Ca^(2+)/calmodulin-dependent protein kinase II Protein kinase A Metabolic syndrome PRE-DIABETES Pre-diabetic cardiomyopathy β-Adrenoceptors 

分 类 号：R587.1[医药卫生—内分泌] R542.2[医药卫生—内科学]