The mitochondria: A target of polyphenols in the treatment of diabetic cardiomyopathy

Abstract

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. © 2020 by the authors. Licensee MDPI, Basel, Switzerland.

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Keywords

Autophagy, Diabetic cardiomyopathy, Polyphenols, Resveratrol, Animals, Apoptosis, Diabetic cardiomyopathies, Humans, Mitochondria, Oxidative stress, Brain natriuretic peptide, Hydroxymethylglutaryl coenzyme a reductase kinase, Janus kinase 1, Polyphenol, Protein bcl 2, Reactive oxygen metabolite, Sirtuin 1, Transcription factor nrf2, Uncoupling protein 2, Ampk signaling, Antiapoptotic activity, Article, Atrial fibrillation, Autophagosome, Biogenesis, Diabetes mellitus, Disease exacerbation, Feedback system, Gene expression, Gene knockdown, Gene silencing, Glucose metabolism, Glucose transport, Heart ventricle remodeling, Human, Hyperglycemia, Lipid metabolism, Lipid oxidation, Mitochondrial biogenesis, Mitochondrial membrane potential, Mitochondrial permeability, Mitochondrial respiration, Mitochondrion, Nonhuman, Protein expression, Protein phosphorylation, Signal transduction, Animal, Drug effect, Metabolism

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