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Signaling in the Aging Heart

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Signaling in the Heart

Abstract

Cardiac aging is a complex multifactorial process not dependent on a unique, singular, pathway, or determined gene(s) or gene products. Rather, a number of specific and nonspecific pathways and genes play a role in the general regulation/modulation of life span, and in particular cardiac aging. Multiple molecular mechanisms interact in cardiac aging either in parallel or in series, including the involvement of somatic mutations, telomere loss, defects in protein turnover, protein functional decline with accumulation of defective proteins (i.e., impaired induction of heat shock proteins and decline in chaperone function), and mitochondrial defects. Most of these mechanisms produce significant damage to cardiac macromolecules.

Mechanisms that appear to play a critical role in aging are the molecular stresses that defective mitochondrial bioenergetics and biogenesis may bring to cardiomyocytes, as well as defects in hormonal and inflammatory signaling and telomere shortening. However, it may not be possible to identify the totality of the mechanisms/pathways that contribute to cardiac aging; intensive research in this regard is currently in process.

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Marín-García, J. (2011). Signaling in the Aging Heart. In: Signaling in the Heart. Springer, Boston, MA. https://doi.org/10.1007/978-1-4419-9461-5_11

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