ArticleJournal of the American Society of Nephrology : JASN2012
Kidney injury accelerates cystogenesis via pathways modulated by heme oxygenase and complement.
Article in Journal of the American Society of Nephrology : JASN, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 43 citations in OpenAlex.
- Immune microenvironment in autosomal dominant polycystic kidney disease.Genes & diseases · 2026Review
- Cytokine-Driven Janus Kinase Signal Transducer and Activator of Transcription Pathway Hyperactivity Predicts Disease Severity in Pediatric FSGS.Kidney360 · 2026Article
- Physiologic mechanisms underlying polycystic kidney disease.Physiological reviews · 2025Review
- Raising serum uric acid with a uricase inhibitor worsens PKD in rat and mouse models.American journal of physiology. Renal physiology · 2024Article
- Reduced decay-accelerating factor expression promotes complement-mediated cystogenesis in murine ADPKD.JCI insight · 2024Article
- The role of complement in kidney disease.Nature reviews. Nephrology · 2023Review
- Pkhd1Journal of molecular medicine (Berlin, Germany) · 2023Article
- Renal injury, biomarkers, and myositis, an understudied aspect of disease: prospective study in the MyoCite cohort.Frontiers in medicine · 2023Article
- Emerging therapies for autosomal dominant polycystic kidney disease with a focus on cAMP signaling.Frontiers in molecular biosciences · 2022Review
- UAB-UCSD O'Brien Center for Acute Kidney Injury Research.American journal of physiology. Renal physiology · 2021Review
- Heme Oxygenase 1: A Defensive Mediator in Kidney Diseases.International journal of molecular sciences · 2021Review
- Role of chemokines, innate and adaptive immunity.Cellular signalling · 2020Review
- Modulation of polycystic kidney disease by G-protein coupled receptors and cyclic AMP signaling.Cellular signalling · 2020Review
- Proteomic Analysis of Urinary Extracellular Vesicles Reveals a Role for the Complement System in Medullary Sponge Kidney Disease.International journal of molecular sciences · 2019Article
- Heterozygous Pkhd1American journal of physiology. Renal physiology · 2019Article
- High glucose-induced complement component 3 up-regulation via RAGE-p38MAPK-NF-κB signalling in astrocytes: In vivo and in vitro studies.Journal of cellular and molecular medicine · 2018Article
- Determinants of Progression in Early Autosomal Dominant Polycystic Kidney Disease: Is it Blood Pressure or Renin-Angiotensin-Aldosterone-System Blockade?Current hypertension reviews · 2018Article
- Heme Oxygenase-1 in Kidney Health and Disease.Antioxidants & redox signaling · 2016Review
- The hallmarks of cancer: relevance to the pathogenesis of polycystic kidney disease.Nature reviews. Nephrology · 2015Review
- Complement activation in progressive renal disease.World journal of nephrology · 2015Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
AKI accelerates cystogenesis. Because cystogenic mutations induce strong transcriptional responses similar to those seen after AKI, these responses may accelerate the progression of cystic renal disease. Here, we modulated the severity of the AKI-like response in Cys1(cpk/cpk) mice, a model that mimics autosomal recessive polycystic kidney disease. Specifically, we induced or inhibited activity of the renoprotective enzyme heme oxygenase (HO) and determined the effects on renal cystogenesis. We found that induction of HO attenuated both renal injury and the rate of cystogenesis, whereas inhibition of HO promoted cystogenesis. HO activity mediated the response of NFκB, which is a hallmark transcriptional feature common to both cystogenesis and AKI. Among the HO-modulated effects we measured, expression of complement component 3 (C3) strongly correlated with cystogenesis, a functionally relevant association as suggested by Cys1(cpk/cpk) mice with genetically induced C3 deficiency. Because both C3 deficiency and HO induction reduce cyst number and cyst areas, these two factors define an injury-stimulated cystogenic pathway that may provide therapeutic targets to slow the formation of new renal cysts and the growth of existing cysts.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.