Cellular senescence is a well-established defensive mechanism for tumor suppression, and is also proposed to play a crucial role in embryonic development, wound repair, aging and age-related diseases. Senescent cell is characterized by the marked morphological changes and active metabolism along with a distinctive senescence associated secretion phenotype (SASP). Cellular senescence is triggered by multiple endogenous and exogenous stressors, which collectively induce three types of senescence. It is believed that senescence represents a programmed phenomenon to facilitate beta cell functional maturation and, therefore, senescence has been suggested to be involved in beta cell regeneration, insulin secretion and diabetes development. Nevertheless, despite past extensive studies, the exact impact of senescence on beta cell viability, regeneration and functionality, and its relevance to the development of diabetes are yet to be fully addressed. In this review, we will summarize the recent progress in beta cell senescence, through which we intend to spark more instructive discussion and perspective with regard to the mechanisms underlying beta cell senescence and their links to the pathogenesis of diabetes and the development of therapeutic strategies.