Level D· Scientific groundwork from lab and animal studiesNarrative ReviewEurope PMCOpen access

Molecular Insights into Ischemia-Reperfusion Injury in Coronary Artery Disease: Mechanisms and Therapeutic Implications: A Comprehensive Review

Ghanta SN., Kattamuri LPV., Odueke A., Mehta JL.

Narrative Review on Cardiovascular Disease, Chronic Inflammation, published in Antioxidants (Basel) (2025) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
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This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Narrative Review
Journal
Antioxidants (Basel) (2025)
Reported sample size
—
Source database
Europe PMC
PMID
40002399
PMCID
PMC11851988
DOI
10.3390/antiox14020213
Citations
10

Abstract (original English)

Coronary artery disease remains a leading cause of morbidity and mortality worldwide. Acute myocardial infarction results in ischemia-induced cellular dysfunction and death. While timely reperfusion limits myocardial damage, it paradoxically triggers ischemia-reperfusion injury (IRI), exacerbating tissue damage. IRI, first observed in the 1960s, is mediated by complex molecular pathways, including oxidative stress, calcium dysregulation, endothelial dysfunction, and inflammation. This review examines emerging therapeutic strategies targeting IRI, including ischemic preconditioning, postconditioning, pharmacological agents, and anti-inflammatory therapies. Preconditioning serves as an endogenous protection mechanism, while pharmacological postconditioning has become a more clinically feasible approach to target oxidative stress, inflammation, and apoptosis during reperfusion. Pharmacological agents, such as GSK-3β inhibitors, JNK inhibitors, and mesenchymal stem cell-derived exosomes, have shown promise in modulating molecular pathways, including Wnt/β-catenin and NF-κB, to reduce myocardial injury and enhance recovery. Combination therapies, integrating pharmacological agents with mechanical postconditioning, provide a synergistic approach to further protect tissue and mitigate damage. However, translating preclinical findings to clinical practice remains challenging due to dis

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is a narrative review: it collects no new patient data and does not systematically appraise evidence quality.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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