Role of Apoptosis in Cardiovascular Diseases: Therapeutic Targets and Strategies

Among noncommunicable diseases, cardiovascular diseases (CVDs) are one of the major contributors to the global death burden. In 2021, it accounted for almost 20.5 million deaths worldwide. Cell death of the cardiomyocytes has been recognized as one of the fundamental incidents that precede heart failure. Ascribed to the resolute job of interminable pumping owing to its constituent cardiomyocyte cells, the heart becomes vulnerable to any injury as these cardiomyocytes are terminally differentiated and are very rarely compensable. Cardiomyocytes primarily die through apoptosis, necrosis, necroptosis, autophagy, pyroptosis, or ferroptosis, the reasons for which can be attributed to the amassed toxic levels of ROS and metabolites that onset a vast array of pathological signaling pathways inside the cells. Adverse ventricular remodeling following cardiac injury during pathological cardiac hypertrophy and myocardial infarction is associated with concomitant cell loss which persuaded researchers to focus on the intricacies of varied forms of cell death in the heart. As CVDs pose a greater threat in the post-COVID era, a precise molecular detailing of the intricacies of the cell death mechanisms would enlighten the cellular milieu of the injured heart that in turn would pave the path for future therapeutic interventions to ameliorate cardiac pathophysiology preceding heart failure.