{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T02:43:43Z","timestamp":1790649823535,"version":"4.1.0"},"reference-count":55,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"5","funder":[{"DOI":"10.13039\/501100005847","name":"Health and Medical Research Fund","doi-asserted-by":"crossref","award":["05161376, Hong Kong Food and Health Bureau"],"award-info":[{"award-number":["05161376, Hong Kong Food and Health Bureau"]}],"id":[{"id":"10.13039\/501100005847","id-type":"DOI","asserted-by":"crossref"}]},{"name":"General Research Fund","award":["14164817"],"award-info":[{"award-number":["14164817"]}]},{"name":"Collaborative Research Fund","award":["C4024-16W"],"award-info":[{"award-number":["C4024-16W"]}]},{"name":"the Hong Kong Research Grants Council"},{"name":"Ministry of Science and Technology of China Research Fund","award":["2018YFC1312704"],"award-info":[{"award-number":["2018YFC1312704"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JASN"],"published-print":{"date-parts":[[2020,5]]},"abstract":"<jats:sec>\n                    <jats:title>Significance Statement<\/jats:title>\n                    <jats:p>\n                      The serine\/threonine kinases MST1 and MST2 are core components of the Hippo pathway, and Yes-associated protein (YAP) is one of the pathway\u2019s main effectors. However, the biologic functions of the Hippo\/YAP pathway in adult kidneys are not well understood, and the role of MST1 and MST2 in the kidney has not been studied. In studies using knockout mice (with tubule-specific deletion of both Mst1 and Mst2) and mouse inner medullary collecting duct cells, the authors demonstrate that tubular deletion of Mst1 and Mst2 activates YAP, which induces inflammation, tubular lesions, fibrosis, and functional impairment; they also show that pathogenesis involves reciprocal stimulation of TNF-\n                      <jats:italic toggle=\"yes\">\u03b1<\/jats:italic>\n                      and YAP signaling activities. Their findings indicate that tubular YAP activation induces renal fibrosis and CKD, thus revealing a novel and critical mechanism underlying this condition.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>The serine\/threonine kinases MST1 and MST2 are core components of the Hippo pathway, which has been found to be critically involved in embryonic kidney development. Yes-associated protein (YAP) and transcriptional coactivator with PDZ-binding motif (TAZ) are the pathway\u2019s main effectors. However, the biologic functions of the Hippo\/YAP pathway in adult kidneys are not well understood, and the functional role of MST1 and MST2 in the kidney has not been studied.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We used immunohistochemistry to examine expression in mouse kidneys of MST1 and MST2, homologs of Hippo in\n                      <jats:italic toggle=\"yes\">Drosophila<\/jats:italic>\n                      . We generated mice with tubule-specific double knockout of Mst1 and Mst2 or triple knockout of Mst1, Mst2, and Yap. PCR array and mouse inner medullary collecting duct cells were used to identify the primary target of Mst1\/Mst2 deficiency.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      MST1 and MST2 were predominantly expressed in the tubular epithelial cells of adult kidneys. Deletion of Mst1\/Mst2 in renal tubules increased activity of YAP but not TAZ. The kidneys of mutant mice showed progressive inflammation, tubular and glomerular damage, fibrosis, and functional impairment; these phenotypes were largely rescued by deletion of Yap in renal tubules. TNF-\n                      <jats:italic toggle=\"yes\">\u03b1<\/jats:italic>\n                      expression was induced\n                      <jats:italic toggle=\"yes\">via<\/jats:italic>\n                      both YAP-dependent and YAP-independent mechanisms, and TNF-\n                      <jats:italic toggle=\"yes\">\u03b1<\/jats:italic>\n                      and YAP amplified the signaling activities of each other in the tubules of kidneys with double knockout of Mst1\/Mst2.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      Our findings show that tubular Mst1\/Mst2 deficiency leads to CKD through both the YAP and non-YAP pathways and that tubular YAP activation induces renal fibrosis. The pathogenesis seems to involve the reciprocal stimulation of TNF-\n                      <jats:italic toggle=\"yes\">\u03b1<\/jats:italic>\n                      and YAP signaling activities.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1681\/asn.2019101052","type":"journal-article","created":{"date-parts":[[2020,4,6]],"date-time":"2020-04-06T17:16:09Z","timestamp":1586193369000},"page":"946-961","source":"Crossref","is-referenced-by-count":56,"title":["Tubule-Specific Mst1\/2 Deficiency Induces CKD via YAP and Non-YAP Mechanisms"],"prefix":"10.1681","volume":"31","author":[{"given":"Chunhua","family":"Xu","sequence":"first","affiliation":[{"name":"School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Li","family":"Wang","sequence":"additional","affiliation":[{"name":"School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yu","family":"Zhang","sequence":"additional","affiliation":[{"name":"School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wenling","family":"Li","sequence":"additional","affiliation":[{"name":"School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jinhong","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Nephrology, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yang","family":"Wang","sequence":"additional","affiliation":[{"name":"School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chenling","family":"Meng","sequence":"additional","affiliation":[{"name":"School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jinzhong","family":"Qin","sequence":"additional","affiliation":[{"name":"The Key Laboratory of Model Animal for Disease Study, Ministry of Education, Model Animal Research Center, Nanjing University, Nanjing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhi-Hua","family":"Zheng","sequence":"additional","affiliation":[{"name":"Department of Nephrology, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4283-9755","authenticated-orcid":false,"given":"Hui-Yao","family":"Lan","sequence":"additional","affiliation":[{"name":"Department of Medicine and Therapeutics, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kingston King-Lun","family":"Mak","sequence":"additional","affiliation":[{"name":"Guangzhou Regenerative Medicine and Health\u2013Guangdong Laboratory, Guangzhou, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yu","family":"Huang","sequence":"additional","affiliation":[{"name":"School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yin","family":"Xia","sequence":"additional","affiliation":[{"name":"School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong, China"},{"name":"Key Laboratory for Regenerative Medicine, Ministry of Education, School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, 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