{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,15]],"date-time":"2026-09-15T11:41:23Z","timestamp":1789472483315,"version":"build-2803163510"},"reference-count":53,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2014,11,25]],"date-time":"2014-11-25T00:00:00Z","timestamp":1416873600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["LUTS"],"published-print":{"date-parts":[[2015,1]]},"abstract":"<jats:p>The incidence of lower urinary tract symptoms, including overactive bladder (<jats:styled-content style=\"fixed-case\">OAB<\/jats:styled-content>), is continuing to rise, and is associated with a negative impact on quality of life and a heavy economic burden. A major risk factor for <jats:styled-content style=\"fixed-case\">OAB<\/jats:styled-content> is advancing age. The etiology of <jats:styled-content style=\"fixed-case\">OAB<\/jats:styled-content> is multifactorial and appears to involve myogenic, neurogenic, and urotheliogenic factors. In this article, we review the strengthening preclinical evidence supporting the contribution of chronic pelvic ischemia to the pathogenesis of <jats:styled-content style=\"fixed-case\">OAB<\/jats:styled-content>. In animal models, chronic ischemia induced by arterial injury and a high\u2010fat diet upregulates markers of oxidative stress and proinflammatory cytokines in the urothelium and lamina propria, and leads to increased expression of nerve growth factor. These processes result in increased afferent activity and an increased frequency of micturition, reflecting a state of bladder hyperactivity. In severe, prolonged cases, bladder overactivity may develop into underactivity. Antimuscarinic therapies are the mainstay of <jats:styled-content style=\"fixed-case\">OAB<\/jats:styled-content> treatment, but their usefulness is limited by modest efficacy and troublesome side\u2010effects. Our increasing understanding of the contribution of chronic ischemia to <jats:styled-content style=\"fixed-case\">OAB<\/jats:styled-content> is leading toward novel therapeutic options targeting chronic pelvic ischemia and its morphological, functional, and oxidative consequences. Preclinical trials have demonstrated encouraging results with \u03b1<jats:sub>1<\/jats:sub>\u2010adrenoreceptor blockade, phosphodiesterase type 5 inhibition, \u03b2<jats:sub>3<\/jats:sub>\u2010adrenoreceptor agonism, free radical scavenging, and stem cell therapy, in preventing morphological, biochemical and functional changes induced by chronic bladder ischemia.<\/jats:p>","DOI":"10.1111\/luts.12084","type":"journal-article","created":{"date-parts":[[2014,11,25]],"date-time":"2014-11-25T08:41:39Z","timestamp":1416904899000},"page":"1-8","source":"Crossref","is-referenced-by-count":31,"title":["Chronic Pelvic Ischemia: Contribution to the Pathogenesis of Lower Urinary Tract Symptoms (<scp>LUTS<\/scp>): A New Target for Pharmacological Treatment?"],"prefix":"10.1111","volume":"7","author":[{"given":"Karl\u2010Erik","family":"ANDERSSON","sequence":"first","affiliation":[{"name":"Wake Forest Institute for Regenerative Medicine, Wake Forest University School of Medicine  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