Although the lack of a robust cardiomyocyte proliferative response has been considered to
be a crucial determinant of cardiac pathology and Heart Failure in adult mammalians, the emerging
picture is that myocardial regeneration is a complex phenotype involving many actors, including acute
cellular senescence and inflammation. However, three major and interconnected events occur in response
to tissue injury: loss of protein homeostasis, accumulation of dysfunctional mitochondria and
chronic inflammation. These events blunt the reparative response of the heart, are associated with the
accumulation of chronically senescent cells and progressively lead to cardiac dysfunction. Therefore, it
is crucial to understand which are the pivotal players of this process, in order to devise strategies aimed at
reducing the occurrence of chronic cell senescence in the heart in vivo.
Keywords: Heart failure, regeneration, cell senescence, proteostasis, mitophagy, inflammation.
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