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Senescent cells accumulate in systemic sclerosis skin
Bo Shi 1, Pei-Suen Tsou 2, Feiyang Ma 3, Michael P Mariani 4, Megan N Mattichak 5, Nathan K LeBrasseur 6, Eduardo N Chini 7, Robert Lafyatis 8, Dinesh Khanna 2, Michael L Whitfield 4, Johann E Gudjonsson 3, John Varga 9
(excerpt below)To the editor, Systemic sclerosis (SSc) is characterized by intractable fibrosis in the skin and internal organs. A unifying paradigm across all forms of fibrosis is transformation of quiescent progenitor cells into activated myofibroblasts, but the pathways underlying transformation and persistence of myofibroblasts in SSc remain poorly understood. SSc might be viewed as an “accelerated aging phenotype”, and SSc patients prematurely display hallmarks of aging including telomere attrition, genomic instability, epigenetic alterations, deregulated nutrient sensing, stem cell exhaustion and mitochondrial dysfunction (Luckhardt and Thannickal, 2015 , Tsou et al., 2022). Cellular senescence is another hallmark of aging. Sustained tissue accumulation of senescent cells is detrimental to organ function, due in part to the senescence-associated secretory phenotype (SASP), characterized by secretion of cytokines/chemokines, growth factors, ECM modifiers, and other substances that promote chronic, "sterile" inflammation and fibrosis.