Heart function protection

Heart function protection, widely termed cardioprotection, refers to the therapeutic objective and physiological process of preserving cardiac structure and performance against pathological insults such as ischemia, oxidative stress, and chronic inflammation [1, 3]. It is not a specific molecular target (e.g., a receptor or enzyme) but rather a clinical outcome resulting from the modulation of various signaling pathways and biological entities [6]. Key mechanisms contributing to this protection include the prevention of cardiomyocyte apoptosis, the inhibition of adverse ventricular remodeling, and the maintenance of mitochondrial integrity and metabolic flexibility [3, 7, 8]. In drug development, heart function protection is mediated by specific molecular targets such as the Angiotensin-converting enzyme (ACE), beta-adrenergic receptors, SGLT2 transporters, and KATP channels [1, 6]. Because 'Heart function protection' describes a functional state or a therapeutic goal, it lacks a unique molecular classification and is considered an incorrect entry for a single molecular target [2, 5].

Other names

CardioprotectionMyocardial protectionCardiac preservationHeart protection

Heart function protection is achieved through diverse pharmacological mechanisms, including the inhibition of the renin-angiotensin-aldosterone system (RAAS), the activation of sarcolemmal KATP channels, the promotion of SERCA2a SUMOylation, the reduction of oxidative stress via Nrf2 pathways, and the modulation of M2 macrophage polarization to reduce inflammation [1, 4, 8].