{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T08:21:59Z","timestamp":1790670119396,"version":"4.1.0"},"reference-count":54,"publisher":"American Physiological Society","issue":"4","funder":[{"DOI":"10.13039\/501100000024","name":"Gouvernement du Canada | Canadian Institutes of Health Research (Instituts de recherche en sant\u00e9 du Canada)","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100000024","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Polycystic Kidney Disease Foundation of Canada"},{"name":"Polycystic Kidney Disease Foundation of USA"},{"name":"Banting and Best Canada Graduate Scholarship Award-CIHR"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2016,10,1]]},"abstract":"<jats:p>Acute kidney injury (AKI) and autosomal dominant polycystic kidney disease (ADPKD) are considered separate entities that both frequently cause renal failure. Since ADPKD appears to depend on a polycystin-1 (Pc1) or Pc2 dosage mechanism, we investigated whether slow progression of cystogenesis in two Pkd1 transgenic mouse models can be accelerated with moderate ischemia-reperfusion injury (IRI). Transient unilateral left ischemic kidneys in both nontransgenic and transgenic mice reproducibly develop tubular dilatations, cysts, and typical PKD cellular defects within 3 mo post-IRI. Similar onset and severity of IRI induced-cystogenesis independently of genotype revealed that IRI is sufficient to promote renal cyst formation; however, this response was not further amplified by the transgene in Pkd1 mouse models. The IRI nontransgenic and transgenic kidneys showed from 16 days post-IRI strikingly increased and sustained Pkd1\/Pc1 (&gt;3-fold) and Pc2 (&gt;8-fold) expression that can individually be cystogenic in mice. In parallel, long-term and important stimulation of hypoxia-inducible factor 1\u03b1 expression was induced as in polycystic kidney disease. While mammalian target of rapamycin signaling is activated, stimulation of the Wnt pathway, with markedly increased active \u03b2-catenin and c-Myc expression in IRI renal epithelium, uncovered a similar regulatory cystogenic response shared by IRI and ADPKD. Our study demonstrates that long-term AKI induces cystogenesis and cross talk with ADPKD Pc1\/Pc2 pathogenic signaling.<\/jats:p>","DOI":"10.1152\/ajprenal.00167.2016","type":"journal-article","created":{"date-parts":[[2016,8,4]],"date-time":"2016-08-04T01:21:01Z","timestamp":1470273661000},"page":"F740-F751","source":"Crossref","is-referenced-by-count":22,"title":["Acute kidney injury induces hallmarks of polycystic kidney disease"],"prefix":"10.1152","volume":"311","author":[{"given":"Almira","family":"Kurbegovic","sequence":"first","affiliation":[{"name":"Molecular Genetics and Development, Institut de Recherches Cliniques de Montr\u00e9al, Facult\u00e9 de M\u00e9decine, Universit\u00e9 de Montr\u00e9al, Montr\u00e9al, Qu\u00e9bec, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marie","family":"Trudel","sequence":"additional","affiliation":[{"name":"Molecular Genetics and Development, Institut de Recherches Cliniques de Montr\u00e9al, Facult\u00e9 de 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