Molecular and imaging biomarkers in myocardial ischemia/reperfusion injury: from pathogenetic mechanisms to therapeutic targeting.

INTRODUCTION

Ischemic heart disease remains a leading cause of morbidity and mortality worldwide despite advances in diagnosis, revascularization, and risk-factor control. Myocardial ischemia/reperfusion (I/R) injury (MIRI) is a multiphase process evolving over minutes to weeks, contributing to infarct expansion, microvascular obstruction, intramyocardial hemorrhage, and adverse ventricular remodeling. High-sensitivity cardiac troponins remain central to diagnosing myocardial necrosis but provide limited mechanistic insight into upstream MIRI processes.

AREAS COVERED: For this review, PubMed/MEDLINE and Scopus were searched from inception to May 2026. Established and emerging biomarkers are examined across the I/R continuum, including tissue-derived markers, inflammatory and oxidative-stress mediators, endothelial and neurohormonal biomarkers, remodeling-related proteins, non-coding RNAs, cell-free DNA, extracellular vesicles, metabolomic and proteomic signatures, and multi-omics platforms. Cardiac magnetic resonance and positron emission tomography are also analyzed for tissue characterization and complication detection.

EXPERT OPINION: The most realistic role for MIRI biomarkers is selective post-reperfusion phenotyping, as high-sensitivity cardiac troponins will remain the diagnostic anchor in acute myocardial infarction. Their initial clinical value is likely prognostic, refining risk stratification and follow-up intensity. Translation will require standardized assays, harmonized sampling, evidence of incremental value, and prospective demonstration that biomarker-guided decisions improve outcomes, resource allocation, cost-effectiveness, and trial efficiency.