©The Author(s) 2021. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Diabetes. Oct 15, 2021; 12(10): 1704-1718
Published online Oct 15, 2021. doi: 10.4239/wjd.v12.i10.1704
Published online Oct 15, 2021. doi: 10.4239/wjd.v12.i10.1704
Tale of two kinases: Protein kinase A and Ca2+/calmodulin-dependent protein kinase II in pre-diabetic cardiomyopathy
Pamela Gaitán-González, Angélica Rueda, Department of Biochemistry, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional, Ciudad de México 07360, Mexico
Rommel Sánchez-Hernández, José-Antonio Arias-Montaño, Department of Physiology, Biophysics and Neurosciences, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional, Ciudad de México 07360, Mexico
Author contributions: Gaitán-González P and Sánchez-Hernández R collected the data, prepared tables, and drafted the manuscript; Arias-Montaño JA and Rueda A designed the review and wrote the manuscript.
Supported by SEP-Cinvestav Project , No. FIDSC 2018/2 ; and SEP-Conacyt Ciencia Básica 2017-2018 , No. A1-S-9082 (to Rueda A) .
Conflict-of-interest statement: Authors declare no conflict of interests for this article.
Corresponding author: Angélica Rueda, PhD, Professor, Department of Biochemistry, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional, Av. IPN 2508, San Pedro Zacatenco, Ciudad de México 07360, Mexico. arueda@cinvestav.mx
Received: February 25, 2021
Peer-review started: February 25, 2021
First decision: June 23, 2021
Revised: July 28, 2021
Accepted: August 30, 2021
Article in press: August 30, 2021
Published online: October 15, 2021
Processing time: 230 Days and 5.6 Hours
Peer-review started: February 25, 2021
First decision: June 23, 2021
Revised: July 28, 2021
Accepted: August 30, 2021
Article in press: August 30, 2021
Published online: October 15, 2021
Processing time: 230 Days and 5.6 Hours
Core Tip
Core Tip: Metabolic syndrome affects heart function leading to pre-diabetic cardiomyopathy. In an attempt to overcome contractility dysfunction, the activity of the sympathetic nervous system increases, but chronic stimulation of β-adrenoceptors leads to alterations in both protein kinase A and Ca2+/calmodulin-dependent protein kinase II activity, the main effectors of the β-adrenergic response. This work recapitulates current evidence about the participation of protein kinase A and Ca2+/calmodulin-dependent protein kinase II in experimental pre-diabetic cardiomyopathy, emphasizing the prevailing role of CaMKII in the development of cardiomyocyte Ca2+ mishandling and myocardial dysfunction associated with pre-diabetes.