{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T00:50:34Z","timestamp":1792025434679,"version":"4.4.0"},"reference-count":71,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"9","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JASN"],"published-print":{"date-parts":[[2018,9]]},"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Increasing evidence indicates that renal recovery from AKI stems from dedifferentiation and proliferation of surviving tubule epithelial cells. Both EGF receptor (EGFR) and the Hippo signaling pathway are implicated in cell proliferation and differentiation, and previous studies showed that activation of EGFR in renal proximal tubule epithelial cells (RPTCs) plays a critical role in recovery from ischemia-reperfusion injury (IRI). In this study, we explored RPTC activation of Yes-associated protein (YAP) and transcriptional coactivator with PDZ binding motif (TAZ), two key downstream effectors of the Hippo pathway, and their potential involvement in recovery from AKI.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We used immunofluorescence to examine YAP expression in kidney biopsy samples from patients with clinical AKI and controls (patients with minimal change disease). Studies of RPTC activation of YAP and TAZ used cultured human RPTCs that were exposed to hypoxia-reoxygenation as well as knockout mice (with inducible deletions of\n                      <jats:italic toggle=\"yes\">Yap<\/jats:italic>\n                      ,\n                      <jats:italic toggle=\"yes\">Taz<\/jats:italic>\n                      , or both occurring specifically in RPTCs) that were subjected to bilateral IRI.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>YAP was activated in RPTCs in kidneys from post-AKI patients and post-IRI mouse kidneys. Inhibition of the interaction of YAP and the TEA domain (TEAD) transcription factor complex by verteporfin or conditional deletion of YAP in RPTCs delayed renal functional and structural recovery from IRI, whereas TAZ deletion had no effect. Activation of the EGFR-PI3K-Akt pathway in response to IRI signaled YAP activation, which promoted cell cycle progression.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>This study shows that EGFR-PI3K-Akt\u2013dependent YAP activation plays an essential role in mediating epithelial cell regeneration during kidney recovery from AKI.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1681\/asn.2017121272","type":"journal-article","created":{"date-parts":[[2018,8,2]],"date-time":"2018-08-02T10:38:39Z","timestamp":1533206319000},"page":"2372-2385","source":"Crossref","is-referenced-by-count":110,"title":["EGF Receptor\u2013Dependent YAP Activation Is Important for Renal Recovery from AKI"],"prefix":"10.1681","volume":"29","author":[{"given":"Jianchun","family":"Chen","sequence":"first","affiliation":[{"name":"Department of Veterans Affairs, Nashville, Tennessee; Departments of"},{"name":"Medicine and"},{"name":"Vanderbilt Center for Kidney Disease, Nashville, Tennessee;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Huaizhou","family":"You","sequence":"additional","affiliation":[{"name":"Medicine and"},{"name":"Division of Nephrology, Huashan Hospital, Fudan University, Shanghai, China; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yan","family":"Li","sequence":"additional","affiliation":[{"name":"Medicine and"},{"name":"Division of Nephrology, Shanghai Ninth People\u2019s Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"You","family":"Xu","sequence":"additional","affiliation":[{"name":"Medicine and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qian","family":"He","sequence":"additional","affiliation":[{"name":"Medicine and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Raymond C.","family":"Harris","sequence":"additional","affiliation":[{"name":"Department of Veterans Affairs, Nashville, Tennessee; Departments of"},{"name":"Medicine and"},{"name":"Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee;"},{"name":"Vanderbilt Center for Kidney Disease, Nashville, Tennessee;"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","published-online":{"date-parts":[[2018,8,2]]},"reference":[{"key":"B1-20230829","first-page":"85","article-title":"Acute kidney injury: Definition, pathophysiology and clinical phenotypes.","volume":"37","author":"Makris","year":"2016","journal-title":"Clin Biochem Rev"},{"key":"B2-20230829","doi-asserted-by":"crossref","first-page":"170","DOI":"10.1016\/S0140-6736(13)60647-9","article-title":"Acute kidney injury: An increasing global concern.","volume":"382","author":"Lameire","year":"2013","journal-title":"Lancet"},{"key":"B3-20230829","doi-asserted-by":"crossref","first-page":"1627","DOI":"10.1056\/NEJMoa0902413","article-title":"Intensity of continuous renal-replacement therapy in critically ill patients.","volume":"361","author":"Bellomo","year":"2009","journal-title":"N Engl J Med"},{"key":"B4-20230829","doi-asserted-by":"crossref","first-page":"7","DOI":"10.1056\/NEJMoa0802639","article-title":"Intensity of renal support in critically ill patients with acute kidney injury.","volume":"359","author":"Palevsky","year":"2008","journal-title":"N Engl J Med"},{"key":"B5-20230829","doi-asserted-by":"crossref","first-page":"4","DOI":"10.1159\/000329027","article-title":"Analysis of the prerenal contributions to acute kidney injury.","volume":"174","author":"Blantz","year":"2011","journal-title":"Contrib Nephrol"},{"key":"B6-20230829","doi-asserted-by":"crossref","first-page":"5","DOI":"10.1172\/JCI200422353","article-title":"Acute renal failure: Definitions, diagnosis, pathogenesis, and therapy.","volume":"114","author":"Schrier","year":"2004","journal-title":"J Clin Invest"},{"key":"B7-20230829","doi-asserted-by":"crossref","first-page":"1796","DOI":"10.1172\/JCI112171","article-title":"Disparate mechanisms for hypoxic cell injury in different nephron segments. 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