Interaction between mitochondrial oxidative stress and myocardial fibrosis in the context of diabetes

Diabetes represents a global chronic health issue and has emerged as a crucial risk factor for cardiovascular diseases (CVD). Myocardial fibrosis (MF), which often accompanies diabetes, plays a pivotal role in the progression of cardiac dysfunction and heart failure (HF). Recent research has highlig...

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Main Authors: Pu-Hua Zhang, Nuo-Nan Li, Xiang Gu, Chun-Xia Zhou, Zhen-Zhen Jiang, Xian-Jun Luo, Hong-Wen Zhu, Xiao-Yong Zhu
Format: Article
Language:English
Published: Frontiers Media S.A. 2025-06-01
Series:Frontiers in Endocrinology
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Online Access:https://www.frontiersin.org/articles/10.3389/fendo.2025.1596436/full
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author Pu-Hua Zhang
Nuo-Nan Li
Nuo-Nan Li
Xiang Gu
Chun-Xia Zhou
Zhen-Zhen Jiang
Xian-Jun Luo
Xian-Jun Luo
Hong-Wen Zhu
Xiao-Yong Zhu
author_facet Pu-Hua Zhang
Nuo-Nan Li
Nuo-Nan Li
Xiang Gu
Chun-Xia Zhou
Zhen-Zhen Jiang
Xian-Jun Luo
Xian-Jun Luo
Hong-Wen Zhu
Xiao-Yong Zhu
author_sort Pu-Hua Zhang
collection DOAJ
description Diabetes represents a global chronic health issue and has emerged as a crucial risk factor for cardiovascular diseases (CVD). Myocardial fibrosis (MF), which often accompanies diabetes, plays a pivotal role in the progression of cardiac dysfunction and heart failure (HF). Recent research has highlighted mitochondrial oxidative stress (OS) as a fundamental mechanism driving MF in diabetic conditions. Elevated blood glucose levels and metabolic imbalances lead to mitochondrial impairments, which in turn cause an excessive buildup of reactive oxygen species (ROS), culminating in OS. This OS not only inflicts direct damage on myocardial cells but also facilitates the proliferation of myocardial fibroblasts and collagen accumulation through the activation of specific signaling pathways, thus intensifying MF. Furthermore, MF itself intensifies mitochondrial OS, creating a vicious cycle that ultimately impairs myocardial structure and function. Thus, a thorough understanding of the interaction between mitochondrial OS and MF in diabetes is crucial for identifying effective therapeutic targets and enhancing the early diagnosis and intervention strategies for diabetic cardiomyopathy.
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issn 1664-2392
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publisher Frontiers Media S.A.
record_format Article
series Frontiers in Endocrinology
spelling doaj-art-5910d79a803c45da8983eb0c5e72e6222025-08-20T03:24:52ZengFrontiers Media S.A.Frontiers in Endocrinology1664-23922025-06-011610.3389/fendo.2025.15964361596436Interaction between mitochondrial oxidative stress and myocardial fibrosis in the context of diabetesPu-Hua Zhang0Nuo-Nan Li1Nuo-Nan Li2Xiang Gu3Chun-Xia Zhou4Zhen-Zhen Jiang5Xian-Jun Luo6Xian-Jun Luo7Hong-Wen Zhu8Xiao-Yong Zhu9Department of Cardiology, Jiujiang University Affiliated Hospital, Jiujiang, Jiangxi, ChinaSchool of Clinical Medicine, Gannan Medical University, Ganzhou, Jiangxi, ChinaJiujiang Clinical Precision Medicine Research Center, Jiujiang, Jiangxi, ChinaDepartment of Cardiology, Jiujiang University Affiliated Hospital, Jiujiang, Jiangxi, ChinaJiujiang Clinical Precision Medicine Research Center, Jiujiang, Jiangxi, ChinaDepartment of Cardiology, Jiujiang University Affiliated Hospital, Jiujiang, Jiangxi, ChinaSchool of Clinical Medicine, Gannan Medical University, Ganzhou, Jiangxi, ChinaJiujiang Clinical Precision Medicine Research Center, Jiujiang, Jiangxi, ChinaDepartment of Cardiology, Jiujiang University Affiliated Hospital, Jiujiang, Jiangxi, ChinaDepartment of Cardiology, Jiujiang University Affiliated Hospital, Jiujiang, Jiangxi, ChinaDiabetes represents a global chronic health issue and has emerged as a crucial risk factor for cardiovascular diseases (CVD). Myocardial fibrosis (MF), which often accompanies diabetes, plays a pivotal role in the progression of cardiac dysfunction and heart failure (HF). Recent research has highlighted mitochondrial oxidative stress (OS) as a fundamental mechanism driving MF in diabetic conditions. Elevated blood glucose levels and metabolic imbalances lead to mitochondrial impairments, which in turn cause an excessive buildup of reactive oxygen species (ROS), culminating in OS. This OS not only inflicts direct damage on myocardial cells but also facilitates the proliferation of myocardial fibroblasts and collagen accumulation through the activation of specific signaling pathways, thus intensifying MF. Furthermore, MF itself intensifies mitochondrial OS, creating a vicious cycle that ultimately impairs myocardial structure and function. Thus, a thorough understanding of the interaction between mitochondrial OS and MF in diabetes is crucial for identifying effective therapeutic targets and enhancing the early diagnosis and intervention strategies for diabetic cardiomyopathy.https://www.frontiersin.org/articles/10.3389/fendo.2025.1596436/fulldiabetesmitochondrial oxidative stressmyocardial fibrosissignaling pathwaysinteractiondrug therapy
spellingShingle Pu-Hua Zhang
Nuo-Nan Li
Nuo-Nan Li
Xiang Gu
Chun-Xia Zhou
Zhen-Zhen Jiang
Xian-Jun Luo
Xian-Jun Luo
Hong-Wen Zhu
Xiao-Yong Zhu
Interaction between mitochondrial oxidative stress and myocardial fibrosis in the context of diabetes
Frontiers in Endocrinology
diabetes
mitochondrial oxidative stress
myocardial fibrosis
signaling pathways
interaction
drug therapy
title Interaction between mitochondrial oxidative stress and myocardial fibrosis in the context of diabetes
title_full Interaction between mitochondrial oxidative stress and myocardial fibrosis in the context of diabetes
title_fullStr Interaction between mitochondrial oxidative stress and myocardial fibrosis in the context of diabetes
title_full_unstemmed Interaction between mitochondrial oxidative stress and myocardial fibrosis in the context of diabetes
title_short Interaction between mitochondrial oxidative stress and myocardial fibrosis in the context of diabetes
title_sort interaction between mitochondrial oxidative stress and myocardial fibrosis in the context of diabetes
topic diabetes
mitochondrial oxidative stress
myocardial fibrosis
signaling pathways
interaction
drug therapy
url https://www.frontiersin.org/articles/10.3389/fendo.2025.1596436/full
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