ABSTRACT
Deformation or failure of organs is the final stage involving fibrosis, caused by fibrous scars composed of excess extracellular matrix proteins. Cellular senescence means a stable stagnation state with no proliferation, during which the senescent cells maintain biochemical metabolism but promote excessive expression of extracellular matrix proteins due to secreting inflammatory factors, which contribute to the development of various organ fibrosis including myocardial fibrosis, and pulmonary fibrosis. It has been shown that both the incidence of organ fibrosis and the number of senescent cells increase with age. This review mainly summarizes mechanisms of cellular senescence and its contribution to the process of various organ fibrosis. Current anti-fibrotic drug therapy focused on cellular senescence is discussed. Cellular senescence has profound implications in the pathogenesis of fibrotic diseases and provides a new target for new effective treatments.