Oxidative Stress in Pancreatic Beta Cell Regeneration

Abstract

Pancreatic β cell neogenesis and proliferation during the neonatal period are critical for the generation of sufficient pancreatic β cell mass/reserve and have a profound impact on long-term protection against type 2 diabetes (T2D). Oxidative stress plays an important role in β cell neogenesis, proliferation, and survival under both physiological and pathophysiological conditions. Pancreatic β cells are extremely susceptible to oxidative stress due to a high endogenous production of reactive oxygen species (ROS) and a low expression of antioxidative enzymes. In this review, we summarize studies describing the critical roles and the mechanisms of how oxidative stress impacts β cell neogenesis and proliferation. In addition, the effects of antioxidant supplements on reduction of oxidative stress and increase of β cell proliferation are discussed. Exploring the roles and the potential therapeutic effects of antioxidants in the process of β cell regeneration would provide novel perspectives to preserve and/or expand pancreatic β cell mass for the treatment of T2D.

Redox regulation in regenerative medicine and tissue engineering: The paradox of oxygen

“…In terms of applications in tissue regeneration, NADPH oxidase also plays an important role in the regeneration of damaged tissues. For example, NADPH oxidase‐dependent ROS formation stimulates the differentiation of murine pancreatic progenitor cells into endocrine cells and thereby enhances pancreatic beta cell regeneration (Liang et al, ) while inhibiting proliferation (Wang & Wang, ). In addition, NADPH oxidase‐induced ROS formation also contributes to the differentiation of cardiomyocytes from embryonic stem cells (Buggisch et al, ).…”

Oxidative Stress and Antioxidant Status in Immune Thrombocytopenia

“…Therefore, the imbalance between oxidant and antioxidant systems is also involved in the pathogenesis of T2D and its complications [22][23][24]. Recent data demonstrates that oxidative stress influences cell-cycle regulators in β cell proliferation and neogenesis [25]. Furthermore, several lines of evidence suggest that oxidative stress is implicated in the pathogenesis of diabetic neuropathy (DSPN) [26].…”

Human mesenchymal stem cells–derived conditioned medium inhibits hypoxia‐induced death of neonatal porcine islets by inducing autophagy

“…Currently, up to 70% of functional islets are destroyed due to hypoxia‐induced damage during the transplantation process . It is well established that pancreatic islets are sensitive to hypoxia and easily become apoptotic and necrotic under hypoxic conditions . Autophagy, a highly conserved catabolic process that captures, degrades, and recycles excess or damaged intracellular contents, promotes cellular homoeostasis and survival .…”