Abstract
Aging imposes a barrier for tissue regeneration. In the heart, aging leads to a severe rearrangement of the cardiac structure and function and to a subsequent increased risk of heart failure. An intricate network of distinct pathways contributes to age-related alterations during healthy heart aging and account for a higher susceptibility of heart disease. Our understanding of the systemic aging process has already led to the design of anti-aging strategies or to the adoption of protective interventions. Nevertheless, our understanding of the molecular determinants operating during cardiac aging or repair remains limited. Here, we will summarize the molecular and physiological alterations that occur during aging of the heart, highlighting the potential role for long non-coding RNAs (lncRNAs) as novel and valuable targets in cardiac regeneration/repair.
Highlights
Worldwide, cardiovascular diseases are the leading cause of death, causing nearly 18 million deaths in 2017
Several long non-coding RNAs (lncRNAs) are expressed during the development of the heart and during heart pathologies
Targeting lncRNAs may be a novel strategy against heart diseases (Bar et al, 2016)
Summary
Cardiovascular diseases are the leading cause of death, causing nearly 18 million deaths in 2017. As opposed to the neonatal heart, adult mammalian hearts lose their capacity to fully regenerate after an exogenous or endogenous harm (Lam and Sadek, 2018) This may be mediated through several interconnected processes, including cellular senescence and secreted factors, telomere attrition, mitochondrial damage, cell death, or inflammation (for a comprehensive review on age-related pathways affecting the heart, see Li et al, 2020a). It is likely that neonatal heart regeneration is mediated by the proliferation of pre-existing cardiomyocytes, and not by cardiac stem or progenitor cells This regenerative state occurs in an extremely short time frame (
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