Abstract
Aging is characterized by a chronic functional decline of organ systems which leads to tissue dysfunction over time, representing a risk factor for diseases development, including cardiovascular. The aging process occurring in the cardiovascular system involves heart and vessels at molecular and cellular level, with subsequent structural modifications and functional impairment. Several modifications involved in the aging process can be ascribed to cellular senescence, a biological response that limits the proliferation of damaged cells. In physiological conditions, the mechanism of cellular senescence is involved in regulation of tissue homeostasis, remodeling, and repair. However, in some conditions senescence-driven tissue repair may fail, leading to the tissue accumulation of senescent cells which in turn may contribute to tumor promotion, aging, and age-related diseases. Cellular reprogramming processes can reverse several age-associated cell features, such as telomere length, DNA methylation, histone modifications and cell-cycle arrest. As such, induced Pluripotent Stem Cells (iPSCs) can provide models of progeroid and physiologically aged cells to gain insight into the pathogenesis of such conditions, to drive the development of new therapies for premature aging and to further explore the possibility of rejuvenating aged cells. An emerging picture is that the tissue remodeling role of cellular senescence could also be crucial for the outcomes of in vivo reprogramming processes. Experimental evidence has demonstrated that, on one hand, senescence represents a cell-autonomous barrier for a cell candidate to reprogramming, but, on the other hand, it may positively sustain the reprogramming capability of surrounding cells to generate fully proficient tissues. This review fits into this conceptual framework by highlighting the most prominent concepts that characterize aging and reprogramming and discusses how the aging tissue might provide a favorable microenvironment for in vivo cardiac reprogramming.
Highlights
In the last decades, developed countries have faced a significant rise in life expectancy with consistent dramatic increase of the elderly population [1].Aging is the major risk factor for cardiovascular diseases, which are the leading cause of morbidity, disability, and death in western countries [2].Reprogramming the Aging HeartThe aging process occurring in the cardiovascular system involves heart and vessels at molecular and cellular level with consequent structural modifications and functional impairment [3].Cardiac aging involves on one hand, cellular macromolecular and mitochondrial and energetic changes and, on the other hand, cell renewal mechanisms and stem cell function
It has been demonstrated that in-vivo reprogramming is facilitated by the accumulation of senescent cells [61]. These results strongly suggest that cell intrinsic and extrinsic effects of senescence can be pivotal for tissue repair and regeneration, during the aging process and in the presence of tissue damage
In vivo lineage reprogramming-based therapies are being considered to treat a wide range of diseases, and tissue-damageinduced senescence seems to contribute to in vivo cellular plasticity via Senescence-Associated Secretory Phenotype (SASP) positively
Summary
Reviewed by: Lucio Barile, Cardiocentro Ticino, Switzerland Manuel M. Aging is characterized by a chronic functional decline of organ systems which leads to tissue dysfunction over time, representing a risk factor for diseases development, including cardiovascular. The aging process occurring in the cardiovascular system involves heart and vessels at molecular and cellular level, with subsequent structural modifications and functional impairment. Several modifications involved in the aging process can be ascribed to cellular senescence, a biological response that limits the proliferation of damaged cells. The mechanism of cellular senescence is involved in regulation of tissue homeostasis, remodeling, and repair. An emerging picture is that the tissue remodeling role of cellular senescence could be crucial for the outcomes of in vivo reprogramming processes. This review fits into this conceptual framework by highlighting the most prominent concepts that characterize aging and reprogramming and discusses how the aging tissue might provide a favorable microenvironment for in vivo cardiac reprogramming
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