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July 1, 2026CellsOpen Access

Oxidative Stress and Its Impact on Reperfused Myocardium: Pathophysiological Insights and Therapeutic Perspectives

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Key result

Targeting oxidative stress in ischemia-reperfusion injury shows experimental promise but faces clinical translation hurdles.

Why the study?

Reperfusion therapy after acute myocardial infarction paradoxically aggravates myocardial injury via oxidative stress, presenting ongoing challenges for clinical translation and cardioprotection.

Design

Review

Authors

IBIris Bararu BojanGrigore T. Popa University of Medicine and PharmacyCPCarmen Elena PleșoianuGrigore T. Popa University of Medicine and PharmacyMVMaria Cristina VladeanuGrigore T. Popa University of Medicine and Pharmacy

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Overview

May reduce MIRI burden in AMI reperfusion; confirms oxidative stress as a modifiable target in RCT evidence.

Key Points

  • This review aims to explore the mechanisms of oxidative stress in myocardial ischemia-reperfusion injury and therapeutic approaches to mitigate its effects.
  • Summarized pathophysiological mechanisms involved in oxidative stress during reperfusion injury.
  • Reviewed current pharmacological and non-pharmacological strategies targeting oxidative stress and inflammation.
  • Discussed emerging evidence on immunometabolic regulation and epigenetic modulation in myocardial ischemia-reperfusion injury.
  • Oxidative stress significantly contributes to myocardial injury post-reperfusion through reactive oxygen and nitrogen species.
  • Mitochondrial dysfunction and inflammatory pathways are key targets for therapeutic intervention to improve cardiac recovery.
  • Challenges in translating experimental findings into clinical practice persist, emphasizing the need for integrated therapeutic strategies.

Structured PICO

P
Population
Patients undergoing reperfusion therapy after acute myocardial infarction and experimental models of myocardial ischemia-reperfusion injury
I
Intervention
Pharmacological and non-pharmacological cardioprotective strategies targeting oxidative stress, mitochondrial dysfunction, and inflammatory signaling

This review provides a comprehensive overview of the molecular mechanisms underlying oxidative stress in myocardial ischemia-reperfusion injury and underscores the need for integrated therapeutic approaches to improve clinical translation.

Cite This Study

Bojan et al. (2026) conducted a review in Myocardial ischemia-reperfusion injury. Oxidative stress acts as a central mechanism in myocardial ischemia-reperfusion injury, with current cardioprotective strategies showing experimental promise but facing clinical translation challenges.

synapsesocial.com/papers/6a44afb45cd2549c8bc44a0fhttps://doi.org/10.3390/cells15131185
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Myocardial Ischemia–Reperfusion Injury—Mechanistic Insights and Novel Therapeutics2026 · 11 citations
  2. 2Myocardial Ischemia/Reperfusion Injury: Molecular Insights, Forensic Perspectives, and Therapeutic Horizons2025 · 31 citations
  3. 3The immune-cardiovascular metabolic circuitry in myocardial ischemia-reperfusion injury: from metabolic signal release to spatiotemporal reprogramming2026
  4. 4Regulatory mechanisms of dynamic mitochondria–macrophage interactions in myocardial ischemia–reperfusion injury and materials-based targeted therapy2026
  5. 5Myocardial Ischemia–Reperfusion Injury: Unraveling Pathophysiology, Clinical Manifestations, and Emerging Prevention Strategies2024 · 27 citations