Cellular signaling pathways regulating β-cell proliferation as a promising therapeutic target in the treatment of diabetes

It is established that a decrease in -cell number and deficiency in the function of existing -cells contribute to type 1 and type 2 diabetes mellitus. Therefore, a major focus of current research is to identify novel methods of improving the number and function of -cells, so as to prevent and/or postpone the development of diabetes mellitus and potentially reverse diabetes mellitus. Based on prior knowledge of the above-mentioned causes, promising therapeutic approaches may include direct transplantation of islets, implantation and subsequent induced differentiation of progenitors/stem cells to -cells, replication of pre-existing -cells, or activation of endogenous -cell progenitors. More recently, with regards to cell replacement and regenerative treatment for diabetes patients, the identification of cellular signaling pathways with related genes or corresponding proteins involved in diabetes has become a topic of interest. However, the majority of pathways and molecules associated with -cells remain unresolved, and the specialized functions of known pathways remain unclear, particularly in humans. The current article has evaluated the progress of research on pivotal cellular signaling pathways involved with -cell proliferation and survival, and their validity for therapeutic adult -cell regeneration in diabetes. More efforts are required to elucidate the cellular events involved in human -cell proliferation in terms of the underlying mechanisms and functions.