Exploring the focal role of pyroptosis in diabetes mellitus

Abstract

Diabetes mellitus is a T cell-mediated disease associated with the depletion of beta cells responsible for insulin production. Although the disease is T cell-mediated, it undergoes various biochemical responses and programmed cell death. Programmed cell death, a distinct biochemical pathway in which cells die by eliciting various physiological outcomes. Pyroptosis, apoptosis, and necrosis are the three major forms of programmed cell death that function as a defense mechanism against various infections, diseases, and microorganisms. This review article focuses on the various pathological mechanisms of pyroptosis. Pyroptosis is distinguished by the caspase-1-dependent formation of plasma membrane pores, resulting in the release of pro-inflammatory cytokines, leading to cell lysis. Caspase-1, a protease which is an interleukin-1L-1β converting enzyme that initiates the cell death process by converting interleukin-1L-1β into mature inflammatory cytokine (mature form). Emerging evidence has made pyroptosis a vital trigger as well as an endogenic regulator of diabetes mellitus.