Oxidative Stress Responses in Cardiovascular Diseases
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: 20 October 2026 | Viewed by 6957
Special Issue Editor
Interests: oxidative stress; cardiology; pharmacology; diabetes; apoptosis; internal medicine; hypertension; antioxidants; reactive oxygen species
Special Issue Information
Dear Colleagues,
It is my pleasure to present this Special Issue to you, which aims to provide a comprehensive overview of the latest research achievements, challenges, and recommendations concerning the unsurpassed and ever-present role of oxidative stress in cardiovascular diseases. As you all know, under physiological conditions, the levels of reactive oxygen species (ROS) production are equivalent to their detoxification, being a major player in cellular signaling and function. In pathological situations, particularly atherosclerosis or hypertension, the release of ROS exceeds endogenous antioxidant capacity, leading to cell death. In the cardiovascular system, oxidative stress is highly implicated in myocardial infarction, ischemia/reperfusion, heart failure, and arrhythmias. However, there are still many discordant findings and questions that impose the need for a deeper understanding of the underlying mechanisms and factors that influence the association between oxidative stress and a wide range of cardiovascular disorders, from the cellular level to clinical outcome. The papers in this Special Issue will therefore make an important contribution to the understanding of this item, whose usefulness in a practical work seems justified. Therefore, original articles based on animal and human investigations, as well as systematic reviews, are more than welcome.
We look forward to your contributions.
Prof. Dr. Vladimir Jakovljevic
Guest Editor
Manuscript Submission Information
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Keywords
- antioxidant capacity
- cardiovascular disease
- cell death
- endothelial dysfunction
- ischemia/reperfusion injury
- oxidative stress
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