ReviewClinical journal of the American Society of Nephrology : CJASN2010
Prospects for mTOR inhibitor use in patients with polycystic kidney disease and hamartomatous diseases.
Review in Clinical journal of the American Society of Nephrology : CJASN, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
52 citing papers in PubMed, 1 synthesis or guideline pooled it, 97 citations in OpenAlex.
- Use of mammalian target of rapamycin inhibitors in patient with autosomal dominant polycystic kidney disease: an updated meta-analysis.International urology and nephrology · 2019Pooled it
- Kidney Cyst Epithelia in Tuberous Sclerosis Complex (TSC) Exhibit Propagation and Expansion of A-Intercalated, but Loss of B-Intercalated and Principal Cells: The Role of FOXI1, FOXP1, and DMRT2 Transcription Factors.International journal of molecular sciences · 2026Article
- Modeling Complex Developmental Disease: The Case of Polycystic Kidney Disease.Journal of developmental biology · 2026Review
- Ketogenic diets in chronic kidney disease patients: a review for skeptics by skeptics.Journal of nephrology · 2025Review
- Activation of toll-like receptor 2 promotes the expression of inflammatory mediators and cell proliferation of human polycystic kidney disease cells.Cellular signalling · 2025Article
- Advances and Challenges in Modeling Autosomal Dominant Polycystic Kidney Disease: A Focus on Kidney Organoids.Biomedicines · 2025Review
- Rapamycin-encapsulated nanoparticle delivery in polycystic kidney disease mice.Scientific reports · 2024Article
- Efficient protocol for the differentiation of kidney podocytes from induced pluripotent stem cells, involving the inhibition of mTOR.Scientific reports · 2023Article
- CaMK4 overexpression in polycystic kidney disease promotes mTOR-mediated cell proliferation.Journal of molecular cell biology · 2022Article
- Cilia-Localized Counterregulatory Signals as Drivers of Renal Cystogenesis.Frontiers in molecular biosciences · 2022Review
- Non-coding RNAs as potential biomarkers and therapeutic targets in polycystic kidney disease.Frontiers in physiology · 2022Review
- Nephronophthisis-Pathobiology and Molecular Pathogenesis of a Rare Kidney Genetic Disease.Genes · 2021Review
- Modeling Neoplastic Growth in Renal Cell Carcinoma and Polycystic Kidney Disease.International journal of molecular sciences · 2021Review
- Hypertension and Prohypertensive Antineoplastic Therapies in Cancer Patients.Circulation research · 2021Review
- Polycystin 2 regulates mitochondrial CaScience signaling · 2019Article
- Aquaporin-3 deficiency slows cyst enlargement in experimental mouse models of autosomal dominant polycystic kidney disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Role of mTOR signaling in the regulation of high glucose-induced podocyte injury.Experimental and therapeutic medicine · 2019Article
- Management of autosomal-dominant polycystic kidney disease-state-of-the-art.Clinical kidney journal · 2018Review
- Renal progression factors in young patients with tuberous sclerosis complex: a retrospective cohort study.Pediatric nephrology (Berlin, Germany) · 2018Article
- Comparison of folate-conjugated rapamycin versus unconjugated rapamycin in an orthologous mouse model of polycystic kidney disease.American journal of physiology. Renal physiology · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 9 institutions in 4 countries.
Funding
Abstract
Mammalian target of rapamycin (mTOR) is the core component of two complexes, mTORC1 and mTORC2. mTORC1 is inhibited by rapamycin and analogues. mTORC2 is impeded only in some cell types by prolonged exposure to these compounds. mTOR activation is linked to tubular cell proliferation in animal models and human autosomal dominant polycystic kidney disease (ADPKD). mTOR inhibitors impede cell proliferation and cyst growth in polycystic kidney disease (PKD) models. After renal transplantation, two small retrospective studies suggested that mTOR was more effective than calcineurin inhibitor-based immunosuppression in limiting kidney and/or liver enlargement. By inhibiting vascular remodeling, angiogenesis, and fibrogenesis, mTOR inhibitors may attenuate nephroangiosclerosis, cyst growth, and interstitial fibrosis. Thus, they may benefit ADPKD at multiple levels. However, mTOR inhibition is not without risks and side effects, mostly dose-dependent. Under certain conditions, mTOR inhibition interferes with adaptive increases in renal proliferation necessary for recovery from injury. They restrict Akt activation, nitric oxide synthesis, and endothelial cell survival (downstream from mTORC2) and potentially increase the risk for glomerular and peritubular capillary loss, vasospasm, and hypertension. They impair podocyte integrity pathways and may predispose to glomerular injury. Administration of mTOR inhibitors is discontinued because of side effects in up to 40% of transplant recipients. Currently, treatment with mTOR inhibitors should not be recommended to treat ADPKD. Results of ongoing studies must be awaited and patients informed accordingly. If effective, lower dosages than those used to prevent rejection would minimize side effects. Combination therapy with other effective drugs could improve tolerability and results.
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What OpenQuestion holds
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.