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Implications of Cellular Aging in Cardiac Reprogramming
Fabiana Passaro1, Gianluca Testa2,3
1Department of Molecular Medicine and Medical Biotechnology, University of Naples "Federico II", Napoli, Italy.
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.
Insights
Cellular senescence, a hallmark of aging, impacts tissue repair and cardiovascular health. This review explores how cellular senescence influences in vivo reprogramming, potentially rejuvenating aged tissues.
Area of Science:
- Gerontology and Regenerative Medicine
- Cardiovascular Biology
- Cellular and Molecular Biology
Background:
- Aging involves progressive functional decline in organ systems, increasing susceptibility to diseases like cardiovascular conditions.
- Cellular senescence, a response to cell damage, contributes to aging and age-related diseases when senescent cells accumulate.
- Cellular reprogramming can reverse age-associated cellular features, offering therapeutic potential for aging and related disorders.
Purpose of the Study:
- To review the interplay between cellular senescence and reprogramming processes in the context of aging.
- To discuss the role of cellular senescence in modulating the microenvironment for in vivo reprogramming, particularly in cardiac tissues.
- To highlight potential therapeutic strategies for premature aging and age-related diseases through cellular rejuvenation.
Main Methods:
- Literature review synthesizing current research on cellular senescence, aging, and cellular reprogramming.
- Analysis of experimental evidence regarding the dual role of senescence as a barrier and facilitator of reprogramming.
- Conceptual framework integrating aging, senescence, and reprogramming for understanding tissue repair and rejuvenation.
Main Results:
- Cellular senescence presents a barrier to reprogramming in individual cells but can create a permissive microenvironment for surrounding cells.
- Senescence-driven tissue remodeling is crucial for the success of in vivo reprogramming processes.
- Aged tissues may offer a favorable microenvironment for in vivo cardiac reprogramming, suggesting potential for rejuvenation therapies.
Conclusions:
- Cellular senescence has a complex, context-dependent role in reprogramming, acting as both an impediment and an enabler.
- Understanding the senescence-reprogramming axis is key to developing strategies for tissue repair and combating age-related decline.
- Targeting cellular senescence and leveraging its effects on reprogramming holds promise for therapeutic interventions in aging and cardiovascular disease.
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