The Mitochondria: A Target of Polyphenols in the Treatment of Diabetic Cardiomyopathy

• Published in: International journal of molecular sciences 2020-07, Vol.21 (14), p.4962
• Main Authors: Bhagani, Humna, Nasser, Suzanne A, Dakroub, Ali, El-Yazbi, Ahmed F, Eid, Assaad A, Kobeissy, Firas, Pintus, Gianfranco, Eid, Ali H
• Format: Article
• Language: English
• Subjects: Adipocytes; Animals; Antioxidants; Apoptosis; Apoptosis - drug effects; Autophagy; Bcl-2 protein; Biosynthesis; Cardiac arrhythmia; Cardiomyocytes; Cardiomyopathy; Cardiovascular disease; Constellations; Cytochrome; Diabetes; Diabetes mellitus; Diabetic Cardiomyopathies - drug therapy; Diabetic Cardiomyopathies - metabolism; diabetic cardiomyopathy; Gene expression; Glucose; Glucose metabolism; Humans; Hyperglycemia; Intermediates; Kinases; Lipid metabolism; Lipids; Metabolism; Metabolites; Mitochondria; Mitochondria - drug effects; Mitochondria - metabolism; Mitochondrial uncoupling protein 2; Oxidative stress; Oxidative Stress - drug effects; Pathogenesis; Peptides; Phagocytosis; Polyphenols; Polyphenols - pharmacology; Polyphenols - therapeutic use; Resveratrol; Review; Therapeutic applications; Ventricle
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms21144962

Diabetic cardiomyopathy (DCM) is a constellation of symptoms consisting of ventricular dysfunction and cardiomyocyte disarray in the presence of diabetes. The exact cause of this type of cardiomyopathy is still unknown; however, several processes involving the mitochondria, such as lipid and glucose metabolism, reactive oxygen species (ROS) production, apoptosis, autophagy and mitochondrial biogenesis have been implicated. In addition, polyphenols have been shown to improve the progression of diabetes. In this review, we discuss some of the mechanisms by which polyphenols, particularly resveratrol, play a role in slowing the progression of DCM. The most important intermediates by which polyphenols exert their protective effect include Bcl-2, UCP2, SIRT-1, AMPK and JNK1. Bcl-2 acts to attenuate apoptosis, UCP2 decreases oxidative stress, SIRT-1 increases mitochondrial biogenesis and decreases oxidative stress, AMPK increases autophagy, and JNK1 decreases apoptosis and increases autophagy. Our dissection of these molecular players aims to provide potential therapeutic targets for the treatment of DCM.