Potassium ion channel (K+ channel) is a crucial transmembrane protein found on cell membranes that plays a pivotal role in regulating various physiological processes such as cell membrane potential, action potential formation, and cellular excitability. Diabetes, a chronic metabolic disorder characterized by elevated blood glucose levels, can cause abnormal changes in the sensitivity and functioning of K+ channels over time. This can lead to an increase in intracellular K+ and Ca2+, disrupting normal cellular function and metabolism and resulting in a range of physiological and metabolic issues. Recent studies have uncovered the collaborative relationship between K+ channels auxiliary SUR1 and Kir6.2 gating, as well as the impact of K+ channel mutations such as KCNK11 Leu114Pro, KCNQ1Arg397Trp, KCNJ11Arg136Cys, KCNK16 Leu114Pro, and KCNMA1 Gly356Arg on diabetes mellitus and associated complications. Specifically, issues such as impaired cardiac repolarization, KATP, Kir, TALK, and KV channel remodeling and a higher risk of arrhythmia have been emphasized. Furthermore, structural and dysfunctional K+ channels (KCa, KV and Kir) can also affect the function of vascular endothelial and smooth muscle cells, leading to impaired vasomotor function, abnormal cell growth, and increased inflammation. These abnormalities can result in cardiovascular damage and lesions, and increase the risk of cardiovascular disease in diabetic individuals. These findings serve as a crucial foundation for a better understanding and addressing cardiovascular issues in patients with diabetes. Moreover, different drugs and treatments targeting the K+ channel may yield varying effects, offering promising prospects for preventing and managing diabetes and its related complications.
Yang et al. (Sat,) studied this question.