ReviewNature reviews. Nephrology2019
The pathobiology of polycystic kidney disease from a metabolic viewpoint.
Review in Nature reviews. Nephrology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
54 citing papers in PubMed, 96 citations in OpenAlex.
- Baseline Characteristics and Patient-Reported Outcomes of ADPKD Patients in the Multicenter TAME-PKD Clinical Trial.Kidney360 · 2020Trial
- RhoA through its various effectors mediate mitochondrial fragmentation in polycystic kidney disease.iScience · 2026Article
- GLIS3, a novel regulator of eicosanoid gene expression and metabolism in normal kidney and polycystic kidney disease.Biochemical pharmacology · 2026Article
- Patient-derived kidney organoids recapitulate ADPKD and facilitate the identification of Rho pathway inhibitors as candidate therapeutics.Cell reports. Medicine · 2026Article
- Sodium-Glucose Cotransporter-2 Inhibitors in ADPKD: Time to Integrate Cardiovascular Outcomes.Kidney international reports · 2026Article
- Regulation of PKM2 expression and function by GLIS3 during metabolic reprogramming in polycystic kidneys.Experimental & molecular medicine · 2026Article
- ift140 -Deficient Zebrafish as a Model for Kidney Cystogenesis and an F0-Based Screen for Genetic Modifiers of Kidney Cysts.Journal of the American Society of Nephrology : JASN · 2026Article
- The Hidden Iceberg of ADPKD: Early Organomegaly-Driven Malnutrition and Sarcopenia Beyond Preserved eGFR.International journal of molecular sciences · 2026Review
- Glomerular Disease and Cystic Kidney Disease: From Pathogenesis to Novel Therapeutic Approaches.Biomedicines · 2025Article
- Review
- Physiologic mechanisms underlying polycystic kidney disease.Physiological reviews · 2025Review
- Microvascular aberrations found in human polycystic kidneys are an early feature in a Pkd1 mutant mouse model.Disease models & mechanisms · 2025Article
- An intronic micro-deletion impacts the transcription and translation ofFrontiers in genetics · 2025Article
- GLIS3: A novel transcriptional regulator of mitochondrial functions and metabolic reprogramming in postnatal kidney and polycystic kidney disease.Molecular metabolism · 2024Article
- Multiomics profiling of mouse polycystic kidney disease progression at a single-cell resolution.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Gene regulatory networks in disease and ageing.Nature reviews. Nephrology · 2024Review
- Reprogramming of Energy Metabolism in HumanInternational journal of molecular sciences · 2024Article
- Myocardin-Related Transcription Factor Mediates Epithelial Fibrogenesis in Polycystic Kidney Disease.Cells · 2024Article
- Mechanistic complement of autosomal dominant polycystic kidney disease: the role of aquaporins.Journal of molecular medicine (Berlin, Germany) · 2024Review
- Multi-omics profiling of mouse polycystic kidney disease progression at a single cell resolution.bioRxiv : the preprint server for biology · 2024Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Autosomal dominant polycystic kidney disease (ADPKD) affects an estimated 1 in 1,000 people and slowly progresses to end-stage renal disease (ESRD) in about half of these individuals. Tolvaptan, a vasopressin 2 receptor blocker, has been approved by regulatory authorities in many countries as a therapy to slow cyst growth, but additional treatments that target dysregulated signalling pathways in cystic kidney and liver are needed. Metabolic reprogramming is a prominent feature of cystic cells and a potentially important contributor to the pathophysiology of ADPKD. A number of pathways previously implicated in the pathogenesis of the disease, such as dysregulated mTOR and primary ciliary signalling, have roles in metabolic regulation and may exert their effects through this mechanism. Some of these pathways are amenable to manipulation through dietary modifications or drug therapies. Studies suggest that polycystin-1 and polycystin-2, which are encoded by PKD1 and PKD2, respectively (the genes that are mutated in >99% of patients with ADPKD), may in part affect cellular metabolism through direct effects on mitochondrial function. Mitochondrial dysfunction could alter the redox state and cellular levels of acetyl-CoA, resulting in altered histone acetylation, gene expression, cytoskeletal architecture and response to cellular stress, and in an immunological response that further promotes cyst growth and fibrosis.
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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.