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Oxidative Stress Unveiled: Mechanisms and Implications in Cardiac Pathologies

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 30 June 2026 | Viewed by 23

Special Issue Editors


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Guest Editor
Department of Pediatrics, Doisy Research Center Saint Louis University, Saint Louis, MO 63104, USA
Interests: cardiomyopathy; cellular metabolism; drug resistance; cell signaling

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Guest Editor
SSM Cardinal Glennon Children’s Hospital, Pediatric Faculty, Saint Louis University, Saint Louis, MO 63104, USA
Interests: role of mitochondrial lipid metabolism in pediatric cardiomyopathies and heart failure

Special Issue Information

Dear Colleagues,

The idea that free radicals contribute to disease can be traced back to Denham Harman’s free radical theory of aging in the 1950s. Since then, oxidative stress (OS) has been increasingly recognized as a central player in cardiovascular disease (CVD). By the 1980s–1990s, research had already begun to shift OS from a physiological messenger to a driver of pathology in heart failure (HF) and ischemia–reperfusion (I/R) injury. OS arises when the balance tips between reactive oxygen species (ROS) and antioxidant defenses. The consequences are profound: DNA damage, lipid peroxidation, protein dysfunction, and ultimately cell death. Mitochondria, NOX enzymes, and neurohormonal pathways fuel ROS production, while conditions like hypertension, diabetes, smoking, and aging exacerbate it. Mitochondrial injury forms a vicious cycle—ROS impair the ETC, damage mtDNA, and open mPTPs, worsening dysfunction. Fibrosis and inflammation follow, with fibroblast activation, cytokine release, and NF-κB signaling reshaping the heart toward stiffness, arrhythmia, and decline in function.

For this Special Issue, we particularly welcome studies exploring paracrine crosstalk between endothelial cells, cardiomyocytes, and fibroblasts, where oxidative stress acts as a signaling mediator in remodeling. We encourage investigations into Nrf2 activation as a master regulator of antioxidant defense, including its interactions with mitochondrial quality control and metabolic adaptation. Genetic insights are also vital, from CYBA polymorphisms in NADPH oxidase to mitochondrial mutations linked to aging-related CVD. Submissions may span diverse models, clinical biomarker studies in patients, transgenic and knockout mouse models, cell-based assays such as H9c2 or iPSCs, zebrafish for dynamic in vivo imaging, and organ-on-chip platforms that capture human-like cardiac microenvironments. Together, these approaches can bring us closer to decoding how oxidative stress shapes the failing heart.

Dr. Sukkum Ngullie Chang
Dr. Vernat Exil
Guest Editors

Manuscript Submission Information

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Keywords

  • reactive oxygen species (ROS)
  • electron transport chain (ETC)
  • mitochondrial permeability transition pore (mPTP)
  • endothelial–cardiomyocyte–fibroblast crosstalk
  • metabolic adaptation
  • inflammation
  • cardiovascular disease (CVD)

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