Therapeutic Approach of Flavonoid in Ameliorating Diabetic Cardiomyopathy by Targeting Mitochondrial-Induced Oxidative Stress
Diabetes cardiomyopathy is one of the key factors of mortality among diabetic patients around the globe. One of the prior contributors to the progression of diabetic cardiomyopathy is cardiac mitochondrial dysfunction. The cardiac mitochondrial dysfunction can induce oxidative stress in cardiomyocyt...
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description | Diabetes cardiomyopathy is one of the key factors of mortality among diabetic patients around the globe. One of the prior contributors to the progression of diabetic cardiomyopathy is cardiac mitochondrial dysfunction. The cardiac mitochondrial dysfunction can induce oxidative stress in cardiomyocytes and was found to be the cause of majority of the heart morphological and dynamical changes in diabetic cardiomyopathy. To slow down the occurrence of diabetic cardiomyopathy, it is crucial to discover therapeutic agents that target mitochondrial-induced oxidative stress. Flavonoid is a plentiful phytochemical in plants that shows a wide range of biological actions against human diseases. Flavonoids have been extensively documented for their ability to protect the heart from diabetic cardiomyopathy. Flavonoids' ability to alleviate diabetic cardiomyopathy is primarily attributed to their antioxidant properties. In this review, we present the mechanisms involved in flavonoid therapies in ameliorating mitochondrial-induced oxidative stress in diabetic cardiomyopathy. |
doi_str_mv | 10.3390/ijms222111616 |
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One of the prior contributors to the progression of diabetic cardiomyopathy is cardiac mitochondrial dysfunction. The cardiac mitochondrial dysfunction can induce oxidative stress in cardiomyocytes and was found to be the cause of majority of the heart morphological and dynamical changes in diabetic cardiomyopathy. To slow down the occurrence of diabetic cardiomyopathy, it is crucial to discover therapeutic agents that target mitochondrial-induced oxidative stress. Flavonoid is a plentiful phytochemical in plants that shows a wide range of biological actions against human diseases. Flavonoids have been extensively documented for their ability to protect the heart from diabetic cardiomyopathy. Flavonoids' ability to alleviate diabetic cardiomyopathy is primarily attributed to their antioxidant properties. In this review, we present the mechanisms involved in flavonoid therapies in ameliorating mitochondrial-induced oxidative stress in diabetic cardiomyopathy.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms222111616</identifier><identifier>PMID: 34769045</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Animals ; Antioxidants ; Cardiomyocytes ; Cardiomyopathy ; Cardiovascular disease ; Chemical compounds ; Diabetes ; Diabetes mellitus ; Diabetic Cardiomyopathies - drug therapy ; Disease prevention ; Energy ; Fatty acids ; Flavonoids ; Flavonoids - pharmacology ; Flavonoids - therapeutic use ; Glucose ; Heart failure ; Humans ; Hyperglycemia ; Insulin ; Kinases ; Metabolism ; Mitochondria ; Mitochondria - drug effects ; Mitochondrial DNA ; Morphology ; Mortality ; Oxidation ; Oxidative stress ; Oxidative Stress - drug effects ; Pathophysiology ; Pharmacology ; Phytochemicals - pharmacology ; Phytochemicals - therapeutic use ; Proteins ; Review</subject><ispartof>International journal of molecular sciences, 2021-10, Vol.22 (21), p.11616</ispartof><rights>2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). 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One of the prior contributors to the progression of diabetic cardiomyopathy is cardiac mitochondrial dysfunction. The cardiac mitochondrial dysfunction can induce oxidative stress in cardiomyocytes and was found to be the cause of majority of the heart morphological and dynamical changes in diabetic cardiomyopathy. To slow down the occurrence of diabetic cardiomyopathy, it is crucial to discover therapeutic agents that target mitochondrial-induced oxidative stress. Flavonoid is a plentiful phytochemical in plants that shows a wide range of biological actions against human diseases. Flavonoids have been extensively documented for their ability to protect the heart from diabetic cardiomyopathy. Flavonoids' ability to alleviate diabetic cardiomyopathy is primarily attributed to their antioxidant properties. 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One of the prior contributors to the progression of diabetic cardiomyopathy is cardiac mitochondrial dysfunction. The cardiac mitochondrial dysfunction can induce oxidative stress in cardiomyocytes and was found to be the cause of majority of the heart morphological and dynamical changes in diabetic cardiomyopathy. To slow down the occurrence of diabetic cardiomyopathy, it is crucial to discover therapeutic agents that target mitochondrial-induced oxidative stress. Flavonoid is a plentiful phytochemical in plants that shows a wide range of biological actions against human diseases. Flavonoids have been extensively documented for their ability to protect the heart from diabetic cardiomyopathy. Flavonoids' ability to alleviate diabetic cardiomyopathy is primarily attributed to their antioxidant properties. 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subjects | Animals Antioxidants Cardiomyocytes Cardiomyopathy Cardiovascular disease Chemical compounds Diabetes Diabetes mellitus Diabetic Cardiomyopathies - drug therapy Disease prevention Energy Fatty acids Flavonoids Flavonoids - pharmacology Flavonoids - therapeutic use Glucose Heart failure Humans Hyperglycemia Insulin Kinases Metabolism Mitochondria Mitochondria - drug effects Mitochondrial DNA Morphology Mortality Oxidation Oxidative stress Oxidative Stress - drug effects Pathophysiology Pharmacology Phytochemicals - pharmacology Phytochemicals - therapeutic use Proteins Review |
title | Therapeutic Approach of Flavonoid in Ameliorating Diabetic Cardiomyopathy by Targeting Mitochondrial-Induced Oxidative Stress |
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