ReviewResults and problems in cell differentiation
Primary Cilia in Cystic Kidney Disease.
Review in Results and problems in cell differentiation. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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
16 citing papers in PubMed, 27 citations in OpenAlex.
- Synchronized temporal-spatial analysis via microscopy and phosphoproteomics (STAMP) of quiescence.Science advances · 2025Article
- Impaired Glucose Metabolism, Primary Cilium Defects, and Kidney Cystogenesis in Glycogen Storage Disease Type Ia.Journal of the American Society of Nephrology : JASN · 2024Article
- Actin cytoskeletal regulation of ciliogenesis in development and disease.Developmental dynamics : an official publication of the American Association of Anatomists · 2024Review
- ALS-linked C9orf72-SMCR8 complex is a negative regulator of primary ciliogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Calcium signaling in polycystic kidney disease- cell death and survival.Cell calcium · 2023Review
- Shortening of primary cilia length is associated with urine concentration in the kidneys.Kidney research and clinical practice · 2023Article
- Nephronophthisis-Pathobiology and Molecular Pathogenesis of a Rare Kidney Genetic Disease.Genes · 2021Review
- Targeting E3 Ubiquitin Ligases and Deubiquitinases in Ciliopathy and Cancer.International journal of molecular sciences · 2020Review
- Epb41l5 interacts with Iqcb1 and regulates ciliary function in zebrafish embryos.Journal of cell science · 2020Article
- Ciliary Genes in Renal Cystic Diseases.Cells · 2020Review
- Cell-Autonomous Hedgehog Signaling Is Not Required for Cyst Formation in Autosomal Dominant Polycystic Kidney Disease.Journal of the American Society of Nephrology : JASN · 2019Article
- Prothymosin α promotes STAT3 acetylation to induce cystogenesis in Pkd1-deficient mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Ciliogenesis associated kinase 1: targets and functions in various organ systems.FEBS letters · 2019Review
- Casein kinase 1ε and 1α as novel players in polycystic kidney disease and mechanistic targets for (R)-roscovitine and (S)-CR8.American journal of physiology. Renal physiology · 2018Article
- Polycystin 1 loss of function is directly linked to an imbalance in G-protein signaling in the kidney.Development (Cambridge, England) · 2018Article
- Cystic Diseases of the Kidneys: From Bench to Bedside.Indian journal of nephrologyReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Primary cilia are small, antenna-like structures that detect mechanical and chemical cues and transduce extracellular signals. While mammalian primary cilia were first reported in the late 1800s, scientific interest in these sensory organelles has burgeoned since the beginning of the twenty-first century with recognition that primary cilia are essential to human health. Among the most common clinical manifestations of ciliary dysfunction are renal cysts. The molecular mechanisms underlying renal cystogenesis are complex, involving multiple aberrant cellular processes and signaling pathways, while initiating molecular events remain undefined. Autosomal Dominant Polycystic Kidney Disease is the most common renal cystic disease, caused by disruption of polycystin-1 and polycystin-2 transmembrane proteins, which evidence suggests must localize to primary cilia for proper function. To understand how the absence of these proteins in primary cilia may be remediated, we review intracellular trafficking of polycystins to the primary cilium. We also examine the controversial mechanisms by which primary cilia transduce flow-mediated mechanical stress into intracellular calcium. Further, to better understand ciliary function in the kidney, we highlight the LKB1/AMPK, Wnt, and Hedgehog developmental signaling pathways mediated by primary cilia and misregulated in renal cystic disease.
Indexed as
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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.