{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T20:23:45Z","timestamp":1791318225401,"version":"4.3.1"},"reference-count":72,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"9","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JASN"],"published-print":{"date-parts":[[2017,9]]},"abstract":"<jats:p>\n                    Autosomal dominant polycystic kidney disease (ADPKD) is characterized by innumerous fluid-filled cysts and progressive deterioration of renal function. Previously, we showed that periostin, a matricellular protein involved in tissue repair, is markedly overexpressed by cyst epithelial cells. Periostin promotes cell proliferation, cyst growth, interstitial fibrosis, and the decline in renal function in PKD mice. Here, we investigated the regulation of these processes by the integrin-linked kinase (ILK), a scaffold protein that links the extracellular matrix to the actin cytoskeleton and is stimulated by periostin. Pharmacologic inhibition or shRNA knockdown of ILK prevented periostin-induced Akt\/mammalian target of rapamycin (mTOR) signaling and ADPKD cell proliferation\n                    <jats:italic toggle=\"yes\">in vitro<\/jats:italic>\n                    . Homozygous deletion of ILK in renal collecting ducts (CD) of\n                    <jats:italic toggle=\"yes\">Ilkfl\/fl<\/jats:italic>\n                    ;\n                    <jats:italic toggle=\"yes\">Pkhd1-Cre<\/jats:italic>\n                    mice caused tubule dilations, apoptosis, fibrosis, and organ failure by 10 weeks of age. By contrast,\n                    <jats:italic toggle=\"yes\">Ilkfl\/+<\/jats:italic>\n                    ;\n                    <jats:italic toggle=\"yes\">Pkhd1-Cre<\/jats:italic>\n                    mice had normal renal morphology and function and survived &gt;1 year. Reduced expression of ILK in\n                    <jats:italic toggle=\"yes\">Pkd1fl\/fl<\/jats:italic>\n                    ;\n                    <jats:italic toggle=\"yes\">Pkhd1-Cre<\/jats:italic>\n                    mice, a rapidly progressive model of ADPKD, decreased renal Akt\/mTOR activity, cell proliferation, cyst growth, and interstitial fibrosis, and significantly improved renal function and animal survival. Additionally, CD-specific knockdown of ILK strikingly reduced renal cystic disease and fibrosis and extended the life of\n                    <jats:italic toggle=\"yes\">pcy\/pcy<\/jats:italic>\n                    mice, a slowly progressive PKD model. We conclude that ILK is critical for maintaining the CD epithelium and renal function and is a key intermediate for periostin activation of signaling pathways involved in cyst growth and fibrosis in PKD.\n                  <\/jats:p>","DOI":"10.1681\/asn.2016111235","type":"journal-article","created":{"date-parts":[[2017,5,18]],"date-time":"2017-05-18T20:40:23Z","timestamp":1495140023000},"page":"2708-2719","source":"Crossref","is-referenced-by-count":42,"title":["Integrin-Linked Kinase Signaling Promotes Cyst Growth and Fibrosis in Polycystic Kidney Disease"],"prefix":"10.1681","volume":"28","author":[{"given":"Archana","family":"Raman","sequence":"first","affiliation":[{"name":"Department of Molecular and Integrative Physiology,"},{"name":"The Kidney Institute, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gail A.","family":"Reif","sequence":"additional","affiliation":[{"name":"The Kidney Institute, and"},{"name":"Internal Medicine and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuqiao","family":"Dai","sequence":"additional","affiliation":[{"name":"The Kidney Institute, and"},{"name":"Internal Medicine and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aditi","family":"Khanna","sequence":"additional","affiliation":[{"name":"The Kidney Institute, and"},{"name":"Internal Medicine and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaogang","family":"Li","sequence":"additional","affiliation":[{"name":"The Kidney Institute, and"},{"name":"Internal Medicine and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lindsay","family":"Astleford","sequence":"additional","affiliation":[{"name":"Internal Medicine and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stephen C.","family":"Parnell","sequence":"additional","affiliation":[{"name":"The Kidney Institute, and"},{"name":"Biochemistry and Molecular Biology, University of Kansas Medical Center, Kansas City, Kansas"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James P.","family":"Calvet","sequence":"additional","affiliation":[{"name":"The Kidney Institute, and"},{"name":"Biochemistry and Molecular Biology, University of Kansas Medical Center, Kansas City, Kansas"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Darren P.","family":"Wallace","sequence":"additional","affiliation":[{"name":"Department of Molecular and Integrative Physiology,"},{"name":"The Kidney Institute, and"},{"name":"Internal Medicine and"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","published-online":{"date-parts":[[2017,5,18]]},"reference":[{"key":"B1-20230819","doi-asserted-by":"crossref","first-page":"699","DOI":"10.1038\/ki.2015.207","article-title":"A polycystin-centric view of cyst formation and disease: The polycystins revisited.","volume":"88","author":"Ong","year":"2015","journal-title":"Kidney 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