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Myocardial injury is a pathological state characterized by damage to heart muscle (myocardium), diagnosed primarily by elevated cardiac biomarkers such as troponins above the clinical reference limit[3][4][6]. It may result from ischemia (as in myocardial infarction), physical trauma (cardiac contusion), inflammation, toxins, or systemic diseases like sepsis and severe anemia[3][7]. The underlying pathobiology can involve acute cell death (necrosis/apoptosis), chronic stress, oxidative injury, inflammation, and the release of molecular signals (DAMPs) that activate pattern recognition receptors, leading to further tissue injury and repair responses[2][10]. Myocardial injury is not a single molecule or drug target but a complex, multifactorial process involving many molecules and signaling pathways.
For drugs affecting myocardial injury indirectly: Anti-ischemic (improve oxygen supply/demand); Antithrombotic (block platelet aggregation/thrombosis); Modulation of apoptosis/necrosis/ferroptosis; Anti-inflammatory pathways.
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