ReviewKidney research and clinical practice2014
Cyst growth, polycystins, and primary cilia in autosomal dominant polycystic kidney disease.
Review in Kidney research and clinical practice, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 49 citations in OpenAlex.
- Autosomal dominant polycystic kidney disease: an overview of recent genetic and clinical advances.Renal failure · 2025Review
- Primary Cilia in Hepatic Biliary Hyperplasia: Implications for Liver Diseases.Seminars in liver disease · 2025Review
- Effects of Pregnancy on Liver and Kidney Cyst Growth Rates in Autosomal Dominant Polycystic Kidney Disease: A Pilot Study.Journal of clinical medicine · 2025Article
- Ultrastructure expansion microscopy (U-ExM) of mouse and human kidneys for analysis of subcellular structures.Cytoskeleton (Hoboken, N.J.) · 2024Article
- A prioritization tool for cilia-associated genes and their in vivo resources unveils new avenues for ciliopathy research.Disease models & mechanisms · 2024Article
- Overexpression of SMYD3 Promotes Autosomal Dominant Polycystic Kidney Disease by Mediating Cell Proliferation and Genome Instability.Biomedicines · 2024Article
- Unraveling the Complexity of Childhood Polycystic Kidney Disease: A Case Study of Three Sisters.Children (Basel, Switzerland) · 2023Article
- Rediscovering Primary Cilia in Pancreatic Islets.Diabetes & metabolism journal · 2023Review
- Characterization of Primary Cilia in Osteoblasts Isolated From Patients With ADPKD and CKD.JBMR plus · 2021Article
- Autosomal dominant polycystic kidney disease and pioglitazone for its therapy: a comprehensive review with an emphasis on the molecular pathogenesis and pharmacological aspects.Molecular medicine (Cambridge, Mass.) · 2020Review
- Ganoderic acid A is the effective ingredient of Ganoderma triterpenes in retarding renal cyst development in polycystic kidney disease.Acta pharmacologica Sinica · 2020Article
- Renal cyst growth is attenuated by a combination treatment of tolvaptan and pioglitazone, while pioglitazone treatment alone is not effective.Scientific reports · 2020Article
- Ciliary exclusion of Polycystin-2 promotes kidney cystogenesis in an autosomal dominant polycystic kidney disease model.Nature communications · 2019Article
- Fibroblast Primary Cilia Are Required for Cardiac Fibrosis.Circulation · 2019Article
- Olfactory Loss and Dysfunction in Ciliopathies: Molecular Mechanisms and Potential Therapies.Current medicinal chemistry · 2019Review
- Polycystic kidney features of the renal pathology in glycogen storage disease type I: possible evolution to renal neoplasia.Journal of inherited metabolic disease · 2018Review
- MicroRNA501-5p induces p53 proteasome degradation through the activation of the mTOR/MDM2 pathway in ADPKD cells.Journal of cellular physiology · 2018Article
- Genetic defects in ciliary genes in autosomal dominant polycystic kidney disease.World journal of nephrology · 2018Article
- Expanding the role of vasopressin antagonism in polycystic kidney diseases: From adults to children?Pediatric nephrology (Berlin, Germany) · 2018Review
- Fluid shear stress-induced TGF-β/ALK5 signaling in renal epithelial cells is modulated by MEK1/2.Cellular and molecular life sciences : CMLS · 2017Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The primary cilium of renal epithelia acts as a transducer of extracellular stimuli. Polycystin (PC)1 is the protein encoded by the PKD1 gene that is responsible for the most common and severe form of autosomal dominant polycystic kidney disease (ADPKD). PC1 forms a complex with PC2 via their respective carboxy-terminal tails. Both proteins are expressed in the primary cilia. Mutations in either gene affect the normal architecture of renal tubules, giving rise to ADPKD. PC1 has been proposed as a receptor that modulates calcium signals via the PC2 channel protein. The effect of PC1 dosage has been described as the rate-limiting modulator of cystic disease. Reduced levels of PC1 or disruption of the balance in PC1/PC2 level can lead to the clinical features of ADPKD, without complete inactivation. Recent data show that ADPKD resulting from inactivation of polycystins can be markedly slowed if structurally intact cilia are also disrupted at the same time. Despite the fact that no single model or mechanism from these has been able to describe exclusively the pathogenesis of cystic kidney disease, these findings suggest the existence of a novel cilia-dependent, cyst-promoting pathway that is normally repressed by polycystin function. The results enable us to rethink our current understanding of genetics and cilia signaling pathways of ADPKD.
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