Abstract
Cellular senescence is a state of irreversible cell cycle arrest in response to an array of cellular stresses. An important role for senescence has been shown for a number of pathophysiological conditions that include cardiovascular disease, pulmonary fibrosis, and diseases of the skin. However, whether senescence contributes to the progression of age-related macular degeneration (AMD) has not been studied in detail so far and the present review describes the recent research on this topic. We present an overview of the types of senescence, pathways of senescence, senescence-associated secretory phenotype (SASP), the role of mitochondria, and their functional implications along with antisenescent therapies. As a central mechanism, senescent cells can impact the surrounding tissue microenvironment via the secretion of a pool of bioactive molecules, termed the SASP. An updated summary of a number of new members of the ever-growing SASP family is presented. Further, we introduce the significance of mechanisms by which mitochondria may participate in the development of cellular senescence. Emerging evidence shows that extracellular vesicles (EVs) are important mediators of the effects of senescent cells on their microenvironment. Based on recent studies, there is reasonable evidence that senescence could be a modifiable factor, and hence, it may be possible to delay age-related diseases by modulating basic aging mechanisms using SASP inhibitors/senolytic drugs. Thus, antisenescent therapies in aging and age-related diseases appear to have a promising potential.
Highlights
Cellular senescence is the irreversible loss of proliferation potential of somatic cells and a variety of associated phenotypic changes that follow [1]
The concept of cellular senescence stems from pioneering studies showing that human diploid fibroblasts have a finite proliferative capacity in culture, despite the fact that they can stay metabolically active even after entering a stable, nondividing stage [2]
retinal pigment epithelium (RPE) senescence is associated with the pathology Macrophage senescence impairs cholesterol efflux and promotes neovascular age-related macular degeneration (AMD) Senescent cells in the outflow pathway; retinal ganglion cell senescence Senescence of retinal ganglion cells Senescence in lens epithelial cells Neurons and blood vessels undergo cellular senescence in the retina Corneal endothelial cells (HCEC) senescence Shortening of telomere length in peripheral leukocytes
Summary
Cellular senescence is the irreversible loss of proliferation potential of somatic cells and a variety of associated phenotypic changes that follow [1]. It was shown that senescence could be induced prematurely by many agents. Several independent studies have shown that senescent cells play a role in multiple biological processes such as embryonic development, wound healing, tissue repair, tumorigenesis, aging, and age-related disease [3]. Studying senescence in the eye and its association with age-related macular degeneration (AMD) will be of great interest. The nature and role of multiple senescence inducers characterized by an array of multiple biomarkers in use as well as mechanisms of cellular senescence are reviewed. The role of mitochondria in cellular senescence with special reference to ocular diseases such as AMD is addressed. The review summarizes available information on senolytic drugs currently used in animal models and in clinical trials
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