ArticleAmerican journal of physiology. Renal physiology2016
Acute kidney injury induces hallmarks of polycystic kidney disease.
Article in American journal of physiology. Renal physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 31 citations in OpenAlex.
- Genomic and epigenomic landscape of ADPKD: towards precision diagnostics and tailored treatments.Frontiers in epigenetics and epigenomics · 2026Review
- Prioritized polycystic kidney disease drug targets and repurposing candidates from pre-cystic and cystic mouse Pkd2 model gene expression reversion.Molecular medicine (Cambridge, Mass.) · 2023Article
- Caspase-1 and the inflammasome promote polycystic kidney disease progression.Frontiers in molecular biosciences · 2022Article
- c-JUN n-Terminal Kinase (JNK) Signaling in Autosomal Dominant Polycystic Kidney Disease.Journal of cellular signaling · 2022Article
- c-Jun N-terminal kinase (JNK) signaling contributes to cystic burden in polycystic kidney disease.PLoS genetics · 2021Article
- Polycystin-1 dependent regulation of polycystin-2 via GRP94, a member of HSP90 family that resides in the endoplasmic reticulum.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Role of chemokines, innate and adaptive immunity.Cellular signalling · 2020Review
- An Overview of In Vivo and In Vitro Models for Autosomal Dominant Polycystic Kidney Disease: A Journey from 3D-Cysts to Mini-Pigs.International journal of molecular sciences · 2020Review
- Cystic renal-epithelial derived induced pluripotent stem cells from polycystic kidney disease patients.Stem cells translational medicine · 2020Article
- Dietary phosphate restriction attenuates polycystic kidney disease in mice.American journal of physiology. Renal physiology · 2020Article
- TMEM33 regulates intracellular calcium homeostasis in renal tubular epithelial cells.Nature communications · 2019Article
- c-Myc is a regulator of the PKD1 gene and PC1-induced pathogenesis.Human molecular genetics · 2019Article
- Clinical Features of 167 Inpatients with Autosomal Dominant Polycystic Kidney Disease at a Single Center in China.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- Environmental hit on a genetic basis in polycystic kidney disease.American journal of physiology. Renal physiology · 2016Article
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2 authors at 2 institutions in 1 country.
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Abstract
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 (>3-fold) and Pc2 (>8-fold) expression that can individually be cystogenic in mice. In parallel, long-term and important stimulation of hypoxia-inducible factor 1α 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 β-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.
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