{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,28]],"date-time":"2026-10-28T03:06:59Z","timestamp":1793156819814,"version":"4.5.0"},"reference-count":249,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2021,6,9]],"date-time":"2021-06-09T00:00:00Z","timestamp":1623196800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"},{"start":{"date-parts":[[2021,6,9]],"date-time":"2021-06-09T00:00:00Z","timestamp":1623196800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["faseb.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The FASEB Journal"],"published-print":{"date-parts":[[2021,7]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Ketamine cystitis (KC) is a chronic bladder inflammation leading to urinary urgency, frequency, and pain. The pathogenesis of KC is complicated and involves multiple tissue injuries in the bladder. Recent studies indicated that urothelium disruption, lamina propria fibrosis and inflammation, microvascular injury, neuropathological alterations, and bladder smooth muscle (BSM) abnormalities all contribute to the pathogenesis of KC. Ketamine has been shown to induce these tissue injuries by regulating different signaling pathways. Ketamine can stimulate antiproliferative factor, adenosine triphosphate, and oxidative stress to disrupt urothelium. Lamina propria fibrosis and inflammation are associated with the activation of cyclooxygenase\u20102, nitric oxide synthase, immunoglobulin E, and transforming growth factor \u03b21. Ketamine contributes to microvascular injury via the\n                    <jats:italic>N<\/jats:italic>\n                    \u2010methyl\u2010D aspartic receptor (NMDAR), and multiple inflammatory and angiogenic factors such as tumor necrosis factor \u03b1 and vascular endothelial growth factor. For BSM abnormalities, ketamine can depress the protein kinase B, extracellular signal\u2010regulated kinase, Cav1.2, and muscarinic receptor signaling. Elevated purinergic signaling also plays a role in BSM abnormalities. In addition, ketamine affects neuropathological alterations in the bladder by regulating NMDAR\u2010 and brain\u2010derived neurotrophic factor\u2010dependent signaling. Inflammatory cells also contribute to neuropathological changes via the secretion of chemical mediators. Clarifying the role and function of these signaling underlying tissue injuries in the bladder with KC can contribute to a better understanding of the pathophysiology of this disease and to the design of effective treatments for KC.\n                  <\/jats:p>","DOI":"10.1096\/fj.202100437","type":"journal-article","created":{"date-parts":[[2021,6,9]],"date-time":"2021-06-09T09:59:55Z","timestamp":1623232795000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":25,"title":["Molecular pathways underlying tissue injuries in the bladder with ketamine cystitis"],"prefix":"10.1096","volume":"35","author":[{"given":"Xiang","family":"Xie","sequence":"first","affiliation":[{"name":"Public Center of Experimental Technology and The School of Basic Medical Sciences Southwest Medical University Luzhou 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