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Molecular Insights into Oxidative-Stress-Mediated Cardiomyopathy and Potential Therapeutic Strategies
Zhenyu Xiong1,2, Yuanpeng Liao1,2, Zhaoshan Zhang1,2
1Department of Vascular and Endovascular Surgery, The First Affiliated Hospital of Yangtze University, Jingzhou 434000, China.
Insights
Oxidative stress (OS) contributes to heart muscle disorders (cardiomyopathies) by damaging heart cells. Targeting OS pathways may offer new treatments for these conditions.
Area of Science:
- Cardiology
- Molecular Biology
- Biochemistry
Background:
- Cardiomyopathies are heart muscle diseases with diverse causes.
- Oxidative stress (OS), an imbalance of reactive oxygen species (ROS), is implicated in cardiomyopathy pathogenesis.
- ROS-mediated damage affects heart structure and function.
Purpose of the Study:
- To synthesize current findings on OS-related signaling pathways in cardiomyopathies.
- To highlight emerging therapeutic targets within redox-regulatory networks.
- To guide the development of antioxidant strategies for improved patient outcomes.
Main Methods:
- Review of existing literature on oxidative stress and cardiomyopathies.
- Analysis of molecular mechanisms linking ROS to cardiac remodeling.
- Identification of potential therapeutic targets in redox pathways.
Main Results:
- OS is a significant factor in hypertrophic, dilated, arrhythmogenic, and stress-induced cardiomyopathies.
- ROS contribute to inflammation, mitochondrial dysfunction, and cardiomyocyte damage.
- Specific redox-regulatory pathways are implicated across different cardiomyopathy subtypes.
Conclusions:
- Understanding OS mechanisms is crucial for treating cardiomyopathies.
- Targeting redox pathways offers potential therapeutic strategies.
- Further research into antioxidant therapies may improve clinical outcomes.
Abstract:
Cardiomyopathies comprise a heterogeneous group of cardiac disorders characterized by structural and functional abnormalities in the absence of significant coronary artery disease, hypertension, valvular disease, or congenital defects. Major subtypes include hypertrophic, dilated, arrhythmogenic, and stress-induced cardiomyopathies. Oxidative stress (OS), resulting from an imbalance between reactive oxygen species (ROS) production and antioxidant defenses, has emerged as a key contributor to the pathogenesis of these conditions. ROS-mediated injury drives inflammation, protease activation, mitochondrial dysfunction, and cardiomyocyte damage, thereby promoting cardiac remodeling and functional decline. Although numerous studies implicate OS in cardiomyopathy progression, the precise molecular mechanisms remain incompletely defined. This review provides an updated synthesis of current findings on OS-related signaling pathways across cardiomyopathy subtypes, emphasizing emerging therapeutic targets within redox-regulatory networks. A deeper understanding of these mechanisms may guide the development of targeted antioxidant strategies to improve clinical outcomes in affected patients.
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