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Abstract Heart failure (HF) is a heterogeneous clinical syndrome that has pathophysiologic manifestations of hemodynamic abnormalities, downstream neurohumoral activation and inflammation, myocardial fibrosis, metabolic dysfunction, and cardiomyocyte injury.
Abstract Programmed cell death (PCD) is a major regulatory mechanism that maintains tissue homeostasis and immune balance and strongly influences the initiation, progression and resolution of inflammation. Although apoptosis, pyroptosis, necroptosis and ferroptosis are individual PCD modes that are regulated by different molecular mechanisms, they are not mutually exclusive in inflammatory microenvironments.
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