Molecular and Cellular Mechanisms of Myocardial Ischemia and Reperfusion Injury: A Narrative Review

Figures

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  Figure 1. Molecular mechanisms of ischemia/reperfusion injury in cardiomyocytes. The figure illustrates the key molecular mechanisms occurring in CMs during I/R injury. During ischemia, a decline in pH, reduced ATP synthesis, and impaired ion pump function create conditions for mitochondrial Ca2+ overload, increased ROS production, and mPTP opening—critical events during the reperfusion phase. Abbreviations: ATP, adenosine triphosphate; CMs, cardiomyocytes; I/R, ischemia/reperfusion; mPTP, mitochondrial permeability transition pore; ROS, reactive oxygen species; SR, sarcoplasmic reticulum.

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  Figure 2. Chronological sequence of molecular events during early reperfusion. The figure represents a time diagram illustrating ionic currents, sources of ROS and the dominance of specific cell death pathways during the early phase of reperfusion. Time frames are based on established data from [19,20,21,22,23,24]. Abbreviations: mPTP, mitochondrial permeability transition pore; NOX, NADPH oxidases; RET, reverse electron transport; ROS, reactive oxygen species; XO, xanthine oxidase.

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  Figure 3. Mechanistic and clinical overview of myocardial ischemia-reperfusion injury. The diagram illustrates key pathophysiological events, current therapeutic approaches, and the assessment of myocardial function. Abbreviations: 2D-STE, two-dimensional speckle tracking echocardiography; ATP, adenosine triphosphate; FT-CMR, feature tracking cardiac magnetic resonance; mPTP, mitochondrial permeability transition pore; PCI, percutaneous coronary intervention; ROS, reactive oxygen species.