ADH5 K113 Lactylation is Associated with Enhanced Glycolysis and Bladder Epithelial Cell Proliferation in Cystitis Glandularis

Background

Cystitis glandularis (CG) is a common inflammatory proliferative disease of the bladder urothelial epithelium. Histologically, it is marked by Brunn 's nest formation and adenoid metaplasia. At present, the molecular mechanism of CG development is not yet clear, and the key signaling pathways regulating the abnormal proliferation of bladder epithelial cells remain to be explored. Lactate, a byproduct of anaerobic glycolysis, serves as a substrate for lactylation, a recently identified post-translational modification, which has been proved to play a regulatory role in inflammatory response and cell proliferation. However, whether this modification occurs in CG bladder epithelial cells and its potential role are still unknown.