Fig. 2.

Acute and chronic effects associated with senescence induction during cardiac injury. Senescent cells accumulate within the ventricular myocardium in response to a range of stressors including myocardial infarction, cardiotoxic medication, systemic neurohormonal changes and increasing age. Senescence particularly in fibroblasts may have a short‐term role in limiting the excessive fibrotic response and improving early angiogenesis. In the chronic setting, senescent cells which are not effectively cleared by the immune system release a SASP which contributes to chronic inflammation, collagen deposition and development of myocardial hypertrophy. Targeting senescent cells in this chronic phase may reduce cardiac dysfunction following myocardial infarction and reduce hypertrophic changes associated with hypertension and ageing. (Figure created with BioRender.com).