Molecular pathways underlying tissue injuries in the bladder with ketamine cystitis

Ketamine cystitis (KC) is a chronic bladder inflammation leading to urinary urgency, frequency, and pain. The pathogenesis of KC complicated involves multiple tissue injuries in the bladder. Recent studies indicated that urothelium disruption, lamina propria fibrosis inflammation, microvascular injury, neuropathological alterations, smooth muscle (BSM) abnormalities all contribute KC. has been shown induce these by regulating different signaling pathways. can stimulate antiproliferative factor, adenosine triphosphate, oxidative stress disrupt urothelium. Lamina are associated with activation cyclooxygenase-2, nitric oxide synthase, immunoglobulin E, transforming growth factor ?1. contributes injury via N-methyl-D aspartic receptor (NMDAR), inflammatory angiogenic factors such as tumor necrosis ? vascular endothelial factor. For BSM abnormalities, ketamine depress protein kinase B, extracellular signal-regulated kinase, Cav1.2, muscarinic signaling. Elevated purinergic also plays role abnormalities. In addition, affects alterations NMDAR- brain-derived neurotrophic factor-dependent Inflammatory cells changes secretion chemical mediators. Clarifying function underlying better understanding pathophysiology this disease design effective treatments for