Senescence is a form of durable cell cycle arrest elicited in response to a wide range of stimuli. Senescent cells remain metabolically active and secrete a variety of factors collectively termed senescence-associated secretory phenotype (SASP). SASP is highly pleiotropic and can impact numerous biological processes in which it has both beneficial and deleterious roles. The underlying mechanisms by which SASP exerts its pleiotropic influence remain largely unknown. SASP serves as an environmental factor, which regulates stem cell differentiation and alters its routine. The latter can potentially be accomplished through dedifferentiation, transdifferentiation, or reprogramming. Behavioral changes that cells undergo when exposed to SASP are involved in several senescence-associated physiological and pathological phenomena. These findings provide clues for identifying possible interventions to reduce the deleterious effects without interfering in the beneficial outcomes. In this study, we discuss the multifaceted effects of SASP and the changes occurring in cellular states upon exposure to SASP factors.

The aging of stem cells impairs the homeostasis in the tissue. Aged stem cells lose their ability to repair tissue and cause the age-related diseases. Senescent microenvironment is one of the important factors which lead to organism aging. The senescence-associated secretory phenotype (SASP) is an important part of senescent microenvironment. The SASP affects the ability of stem cells to repair and drives the process of aging. Extracellular vesicles (EVs) are thought to play an important role in senescent microenvironment. EVs secreted by senescent cells carry non-coding RNA such as mi RNAs and a variety of active molecules including SASP, which are involved in the regulation of senescent microenvironment. This paper reviews the reasons of the stem cells aging and the research progress of senescent microenvironment, so as to provide the experimental basis and theoretical basis for the clinical application of stem cells.