{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,27]],"date-time":"2026-08-27T22:01:55Z","timestamp":1787868115589,"version":"build-2784847793"},"reference-count":86,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2024,7,3]],"date-time":"2024-07-03T00:00:00Z","timestamp":1719964800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Neurol."],"abstract":"<jats:p>\n                    Cumulative evidence suggests that ATP-sensitive potassium (K\n                    <jats:sub>ATP<\/jats:sub>\n                    ) channels act as a key regulator of cerebral blood flow (CBF). This implication seems to be complicated, since K\n                    <jats:sub>ATP<\/jats:sub>\n                    channels are expressed in several vascular-related structures such as smooth muscle cells, endothelial cells and pericytes. In this systematic review, we searched PubMed and EMBASE for preclinical and clinical studies addressing the involvement of K\n                    <jats:sub>ATP<\/jats:sub>\n                    channels in CBF regulation. A total of 216 studies were screened by title and abstract. Of these, 45 preclinical and 6 clinical studies were included. Preclinical data showed that K\n                    <jats:sub>ATP<\/jats:sub>\n                    channel openers (KCOs) caused dilation of several cerebral arteries including pial arteries, the middle cerebral artery and basilar artery, and K\n                    <jats:sub>ATP<\/jats:sub>\n                    channel inhibitor (KCI) glibenclamide, reversed the dilation. Glibenclamide affected neither the baseline CBF nor the baseline vascular tone. Endothelium removal from cerebral arterioles resulted in an impaired response to KCO\/KCI. Clinical studies showed that KCOs dilated cerebral arteries and increased CBF, however, glibenclamide failed to attenuate these vascular changes. Endothelial K\n                    <jats:sub>ATP<\/jats:sub>\n                    channels played a major role in CBF regulation. More studies investigating the role of K\n                    <jats:sub>ATP<\/jats:sub>\n                    channels in CBF-related structures are needed to further elucidate their actual role in cerebral hemodynamics in humans.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Systematic review registration:<\/jats:bold>\n                    Prospero: CRD42023339278 (preclinical data) and CRD42022339152 (clinical data).\n                  <\/jats:p>","DOI":"10.3389\/fneur.2024.1417421","type":"journal-article","created":{"date-parts":[[2024,7,3]],"date-time":"2024-07-03T01:32:55Z","timestamp":1719970375000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":4,"title":["KATP channels in cerebral hemodynamics: a systematic review of preclinical and clinical studies"],"prefix":"10.3389","volume":"15","author":[{"given":"Hassan Ali Suleiman","family":"Daoud","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lili","family":"Kokoti","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mohammad Al-Mahdi","family":"Al-Karagholi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2024,7,3]]},"reference":[{"key":"ref1","doi-asserted-by":"publisher","first-page":"031411","DOI":"10.1117\/1.NPh.3.3.031411","article-title":"Cerebral blood flow and autoregulation: current measurement techniques and prospects for noninvasive optical methods","volume":"3","author":"Fantini","year":"2016","journal-title":"Neurophotonics"},{"key":"ref2","doi-asserted-by":"publisher","first-page":"161","DOI":"10.1016\/j.expneurol.2014.10.003","article-title":"Neuronal KATP channels mediate hypoxic preconditioning and reduce subsequent neonatal 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