Commentary - Journal of Clinical Endocrinology Research (2025) Volume 8, Issue 1

Addressing oxidative stress-induced cardiovascular dysfunctions: A perspective on therapeutic strategies.

Ademola Adetokunbo Oyagbemi ^*

Department of Veterinary Physiology, Biochemistry and Pharmacology, University of Ibadan, Ibadan, Nigeria

Corresponding Author:

Ademola Adetokunbo Oyagbemi
Department of Veterinary Physiology
Biochemistry and Pharmacology, University of Ibadan, Ibadan, Nigeria
E-mail: ademola.oyagbemi178@gmail.com

Received: 05-Apr-2024, Manuscript No. AAJCER-24-131477; Editor assigned: 07-Apr-2024, AAJCER-24-131477 (PQ); Reviewed: 20-Apr-2024, QC No. AAJCER-24-131477; Revised: 07-Apr-2025, Manuscript No. AAJCER-24-131477 (R); Published: 14-Apr-2025, DOI: 10.35841/AAJCER.8.1.180

Citation: Oyagbemi AA. Addressing oxidative stress-induced cardiovascular dysfunctions: A perspective on therapeutic strategies. J Clin Endocrinol Res. 2025;8(1):180

Introduction

Oxidative stress is a pivotal contributor to the pathogenesis of various cardiovascular disorders, including hypertension, atherosclerosis, and heart failure. Excessive production of Reactive Oxygen Species (ROS) overwhelms endogenous antioxidant defenses, leading to endothelial dysfunction, inflammation, and tissue damage. In this perspective article, we explore the intricate mechanisms of oxidative stress-induced cardiovascular dysfunctions and discuss emerging therapeutic strategies aimed at mitigating oxidative damage and preserving cardiovascular health.

Understanding oxidative stress in cardiovascular pathophysiology

Oxidative stress arises from an imbalance between ROS generation and antioxidant capacity within the cardiovascular system. ROS, such as superoxide anion (O₂•⁻), hydrogen peroxide (H₂O₂), and hydroxyl radical (•OH), are produced by various enzymatic and non-enzymatic pathways, including NADPH oxidases, mitochondria, and uncoupled Endothelial Nitric Oxide Synthase (eNOS). Under physiological conditions, ROS serve as signaling molecules involved in vascular homeostasis and cellular signaling. However, dysregulation of ROS production or impaired antioxidant defenses can lead to oxidative damage to lipids, proteins, and DNA, promoting the development and progression of cardiovascular diseases.

Therapeutic approaches targeting oxidative stress

Several therapeutic strategies have been proposed to counteract oxidative stress-induced cardiovascular dysfunctions:

Antioxidant therapy: Administration of exogenous antioxidants, such as vitamins C and E, coenzyme Q10, and polyphenols, aims to scavenge ROS and restore redox balance. However, clinical trials investigating the efficacy of antioxidant supplements in cardiovascular disease prevention have yielded mixed results, highlighting the need for further research to elucidate optimal dosing regimens and patient selection criteria.

Activation of endogenous antioxidant defense systems: Strategies to enhance endogenous antioxidant defenses involve targeting key enzymes and transcription factors involved in antioxidant gene expression. Agents such as Nuclear Factor Erythroid 2-Related Factor 2 (Nrf2) activators and Heme Oxygenase-1 (HO-1) inducers have shown promise in preclinical studies by upregulating antioxidant enzyme expression and protecting against oxidative stress-induced cardiovascular injury.

Mitochondrial protection: Mitochondria are major sources of ROS production and targets of oxidative damage in cardiovascular diseases. Therapeutic interventions aimed at preserving mitochondrial function and integrity, such as mitochondrial-targeted antioxidants and mitophagy inducers, hold potential for mitigating oxidative stress-induced cardiovascular dysfunctions and improving cardiac outcomes.

Lifestyle modifications: Lifestyle interventions, including regular physical activity, dietary modifications, and smoking cessation, play a crucial role in reducing oxidative stress and improving cardiovascular health. Exercise training enhances antioxidant defenses, promotes vascular function, and attenuates oxidative damage, while a diet rich in antioxidants and omega-3 fatty acids confers cardio protective effects.

Conclusion

Oxidative stress-induced cardiovascular dysfunctions represent a significant therapeutic challenge in modern medicine. While antioxidant therapies have shown promise in preclinical studies, their clinical efficacy remains uncertain, underscoring the need for further research to identify novel therapeutic targets and optimize treatment strategies. A multifaceted approach targeting oxidative stress at multiple levels, including antioxidant therapy, activation of endogenous defense systems, mitochondrial protection, and lifestyle modifications, holds promise for combating oxidative stress-induced cardiovascular diseases and improving patient outcomes in the future.