{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,12]],"date-time":"2026-08-12T15:39:28Z","timestamp":1786549168685,"version":"build-2736575974"},"reference-count":56,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"5","funder":[{"DOI":"10.13039\/501100000291","name":"Kidney Research UK","doi-asserted-by":"crossref","award":["INT_009_20191202"],"award-info":[{"award-number":["INT_009_20191202"]}],"id":[{"id":"10.13039\/501100000291","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100010269","name":"Wellcome Trust","doi-asserted-by":"crossref","award":["226804\/Z\/22\/Z"],"award-info":[{"award-number":["226804\/Z\/22\/Z"]}],"id":[{"id":"10.13039\/100010269","id-type":"DOI","asserted-by":"crossref"}]},{"name":"NIH","award":["R01-DK119212"],"award-info":[{"award-number":["R01-DK119212"]}]},{"name":"Department of Veterans Affairs Merit Review","award":["1I01BX002025"],"award-info":[{"award-number":["1I01BX002025"]}]},{"name":"Wellcome Center for Cell-Matrix Research","award":["203128\/A\/16\/Z"],"award-info":[{"award-number":["203128\/A\/16\/Z"]}]},{"name":"Department of Veterans Affairs Senior Research Career Scientist Award","award":["IK6 BX005240"],"award-info":[{"award-number":["IK6 BX005240"]}]}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":["JASN"],"published-print":{"date-parts":[[2026,5]]},"abstract":"\n Key Points<\/jats:title>\n \n \n \n \n Multiomic analysis of the\n Pkd1<\/jats:italic>\n nl\/nl<\/jats:sup>\n mouse and human autosomal dominant polycystic kidney disease tissue identified upregulation of integrin-\n \u03b1<\/jats:italic>\n 1.\n <\/jats:p>\n <\/jats:list-item>\n \n \n Global knockout of integrin subunit\n \u03b1<\/jats:italic>\n 1 reduced kidney cyst size and preserved kidney function.\n <\/jats:p>\n <\/jats:list-item>\n \n \n Loss of integrin-\n \u03b1<\/jats:italic>\n 1 in\n Pkd1<\/jats:italic>\n nl\/nl<\/jats:sup>\n mice precluded interstitial fibrosis, which we suggest was due to reduced fibroblast cell proliferation.\n <\/jats:p>\n <\/jats:list-item>\n <\/jats:list>\n <\/jats:p>\n <\/jats:sec>\n \n Background<\/jats:title>\n Cystogenesis and interstitial fibrosis are contributing factors to kidney failure in individuals with autosomal dominant polycystic kidney disease (ADPKD). The molecular and cellular mechanisms involved in cyst growth and fibrosis are complex, and new therapies are urgently needed to improve clinical outcomes.<\/jats:p>\n <\/jats:sec>\n \n Methods<\/jats:title>\n \n We used mass spectrometry\u2013based proteomics to identify molecular changes in the\n Pkd1<\/jats:italic>\n nl\/nl<\/jats:sup>\n mouse model of ADPKD and selected integrin-\n \u03b1<\/jats:italic>\n 1 as a candidate of interest to follow-up in functional studies. Mice lacking integrin-\n \u03b1<\/jats:italic>\n 1 (\n Itga1<\/jats:italic>\n \u2212\/\u2212<\/jats:sup>\n ) were crossed to\n Pkd1<\/jats:italic>\n nl\/nl<\/jats:sup>\n mice, and effects on kidney function and kidney histology were measured. We investigated the effects of integrin-\n \u03b1<\/jats:italic>\n 1 depletion on fibrosis markers using quantitative RT-PCR, Western blot, and immunofluorescence.\n <\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n Proteomic analysis of the\n Pkd1<\/jats:italic>\n nl\/nl<\/jats:sup>\n mouse showed increased abundance of integrin-\n \u03b1<\/jats:italic>\n 1. In human ADPKD tissue and two single-cell RNA kidney disease datasets,\n ITGA1<\/jats:italic>\n was also upregulated. To investigate the functional role of this integrin subunit in ADPKD, we generated a\n Pkd1<\/jats:italic>\n nl\/nl<\/jats:sup>\n Itga1<\/jats:italic>\n \u2212\/\u2212<\/jats:sup>\n mouse. We observed a significant reduction in kidney volume and kidney dysfunction in\n Pkd1<\/jats:italic>\n nl\/nl<\/jats:sup>\n mice lacking integrin-\n \u03b1<\/jats:italic>\n 1. Kidneys from\n Pkd1<\/jats:italic>\n nl\/nl<\/jats:sup>\n Itga1<\/jats:italic>\n \u2212\/\u2212<\/jats:sup>\n mice had smaller cysts, reduced interstitial expansion, and less tubular atrophy. The myofibroblast marker\n \u03b1<\/jats:italic>\n -smooth muscle actin remained switched on in Pdgfrb\n +<\/jats:sup>\n stromal cells of\n Pkd1<\/jats:italic>\n nl\/nl<\/jats:sup>\n Itga1<\/jats:italic>\n \u2212\/\u2212<\/jats:sup>\n kidneys, suggesting that integrin-\n \u03b1<\/jats:italic>\n 1 is not needed for activation of fibroblasts. Analysis of cell proliferation markers suggested that integrin-\n \u03b1<\/jats:italic>\n 1 promoted fibroblast expansion in response to cystic injury.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions<\/jats:title>\n \n These results highlight a previously unrecognized role for integrin-\n \u03b1<\/jats:italic>\n 1 in cyst growth and fibrosis in PKD.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1681\/asn.0000000941","type":"journal-article","created":{"date-parts":[[2025,12,3]],"date-time":"2025-12-03T13:00:20Z","timestamp":1764766820000},"page":"959-973","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":1,"title":["Integrin \u03b11\u03b21 Promotes Interstitial Fibrosis and Cyst Growth in a Mouse Model of Polycystic Kidney Disease"],"prefix":"10.1681","volume":"37","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4521-9404","authenticated-orcid":false,"given":"Celine","family":"Grenier","sequence":"first","affiliation":[{"name":"Division of Cell-Matrix Biology and Regenerative Medicine, Manchester Cell-Matrix Centre, Faculty of Biology Medicine and Health, School of Biological Sciences, The University of Manchester, Manchester, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6207-1299","authenticated-orcid":false,"given":"I-Hsuan","family":"Lin","sequence":"additional","affiliation":[{"name":"Bioinformatics Core Facility, Faculty of Biology Medicine and Health, The University of Manchester, Manchester, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6974-7143","authenticated-orcid":false,"given":"Dorien J.M.","family":"Peters","sequence":"additional","affiliation":[{"name":"Department of Human Genetics, Leiden University Medical Center, Leiden, The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8502-1481","authenticated-orcid":false,"given":"Ambra","family":"Pozzi","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension, Department of Medicine, Vanderbilt University, Nashville, Tennessee"},{"name":"Department of Veterans Affairs, Vanderbilt University, Nashville, Tennessee"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6400-0227","authenticated-orcid":false,"given":"Rachel","family":"Lennon","sequence":"additional","affiliation":[{"name":"Division of Cell-Matrix Biology and Regenerative Medicine, Manchester Cell-Matrix Centre, Faculty of Biology Medicine and Health, School of Biological Sciences, The University of Manchester, Manchester, United 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