• Stimulants such as oxidation and endoplasmice stress, DNA damage, epigenetic modification, etc., stimulate. • Stress response, classical senescence proteins, CCHOP, calcineurin/CaMKII, etc., • Promoting senescence and dead cells accumulation, endocardium remodeling. • Accelerating contractile dysfunction, impaired left ventricular ejection fraction and HF in aging population. • However, attenuating senescence and dead cell retention prevents cardiac aging and HF development. [ABSTRACT FROM AUTHOR]