ArticleNature communications2023
The C-terminal tail of polycystin-1 suppresses cystic disease in a mitochondrial enzyme-dependent fashion.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 39 citations in OpenAlex.
- RhoA through its various effectors mediate mitochondrial fragmentation in polycystic kidney disease.iScience · 2026Article
- Evidence for a tubular basement membrane-cilia connection in autosomal dominant polycystic kidney disease pathogenesis.The Journal of clinical investigation · 2026Article
- Modeling Complex Developmental Disease: The Case of Polycystic Kidney Disease.Journal of developmental biology · 2026Review
- Review
- Polycystin-1 and Cardiac Remodeling: From Mechanotransduction to Clinical Consequences.Circulation research · 2026Review
- The Role of Mitochondria in Polycystic Kidney Disease.International journal of molecular sciences · 2026Review
- Commemorating the National Institute of Diabetes and Digestive and Kidney Diseases' Advances in Kidney Health: 75 Years of Discovery and Impact.Journal of the American Society of Nephrology : JASN · 2026Article
- EGR1 Nuclear Condensates Promote Renal Cyst Development in Polycystic Kidney Disease.Exploration (Beijing, China) · 2026Article
- Recapitulating Liver Embryology-Lessons to Be Learned for Liver Diseases.Journal of developmental biology · 2025Review
- Physiological functions and pharmacological targeting of transient receptor potential channels.Pharmacological reviews · 2025Review
- Endoplasmic reticulum-mediated organelle crosstalk in kidney disease.Nature reviews. Nephrology · 2025Review
- Commemorating the National Institute of Diabetes and Digestive and Kidney Diseases' Advances in Kidney Health: 75 Years of Discovery and Impact.Clinical journal of the American Society of Nephrology : CJASN · 2025Article
- Therapies in autosomal dominant polycystic kidney disease: beyond tolvaptan.Current opinion in nephrology and hypertension · 2025Review
- Physiologic mechanisms underlying polycystic kidney disease.Physiological reviews · 2025Review
- Metabolic Reprogramming in Autosomal Dominant Polycystic Kidney Disease: Role in Cystogenesis and Novel Therapeutic Approaches.Biomedicines · 2025Review
- Metabolic reprogramming in polycystic kidney disease and other renal ciliopathies.EMBO molecular medicine · 2025Review
- Novel PKD1 Mutation (c.G10086T) Drives High Intracranial Aneurysm Risk in Autosomal Dominant Polycystic Kidney Disease.European journal of neurology · 2025Article
- Prospects for gene therapy in polycystic kidney disease.Current opinion in nephrology and hypertension · 2025Review
- Genome-Based Advances in Modeling Renal Ciliopathies and Enhancing Patient Care.Kidney & blood pressure research · 2025Review
- Eliosin-an alternative product from the HmPKD1 locus is a component of endoplasmic reticulum mitochondria membrane contact sites.PloS one · 2025Article
Corrections and comments
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Authors and funding
15 authors at 2 institutions in 1 country.
Funding
Abstract
Autosomal dominant polycystic kidney disease (ADPKD) is the most prevalent potentially lethal monogenic disorder. Mutations in the PKD1 gene, which encodes polycystin-1 (PC1), account for approximately 78% of cases. PC1 is a large 462-kDa protein that undergoes cleavage in its N and C-terminal domains. C-terminal cleavage produces fragments that translocate to mitochondria. We show that transgenic expression of a protein corresponding to the final 200 amino acid (aa) residues of PC1 in two Pkd1-KO orthologous murine models of ADPKD suppresses cystic phenotype and preserves renal function. This suppression depends upon an interaction between the C-terminal tail of PC1 and the mitochondrial enzyme Nicotinamide Nucleotide Transhydrogenase (NNT). This interaction modulates tubular/cyst cell proliferation, the metabolic profile, mitochondrial function, and the redox state. Together, these results suggest that a short fragment of PC1 is sufficient to suppress cystic phenotype and open the door to the exploration of gene therapy strategies for ADPKD.
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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.