Evidence map›Paper›PMID 24861210›Full record

ReviewBirth defects research. Part C, Embryo today : reviews2014

Developmental signaling: does it bridge the gap between cilia dysfunction and renal cystogenesis?

Pamela V Tran, Madhulika Sharma, Xiaogang Li, James P Calvet

Open access · greenAbstract readReview
In one paragraph

Review in Birth defects research. Part C, Embryo today : reviews, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
3.0field-weighted citation impact, top 9% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed, 22 citations in OpenAlex.

  1. Diseases of the primary cilia: a clinical characteristics review.Pediatric nephrology (Berlin, Germany) · 2025
    Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. The regulatory 1α subunit of protein kinase A modulates renal cystogenesis.American journal of physiology. Renal physiology · 2017
    Article
  9. Article
  10. Article
  11. Review
  12. Primary Cilia in Cystic Kidney Disease.Results and problems in cell differentiation
    Review
  13. Kidney: polycystic kidney disease.Wiley interdisciplinary reviews. Developmental biology
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Pamela V TranDepartment of Anatomy and Cell Biology, University of Kansas Medical Center, Kansas City, Kansas; The Kidney Institute, University of Kansas Medical Center, Kansas City, Kansas.
Madhulika Sharma
Xiaogang Li
James P Calvet
University of Kansas Medical Center · US

Funding

Transgenic and Gener-Targeting CoreP20GM104936 · NIGMS · UNIVERSITY OF KANSAS MEDICAL CENTER · PI SAADI, IRFAN · 2012 to 2016
$10.9M
ADPKD: Understanding mechanisms, Discovering treatments.R01DK084097 · NIDDK · UNIVERSITY OF KANSAS MEDICAL CENTER · PI LI, XIAOGANG · 2010 to 2018
$2.3M
THM1 modulation of GLI2 activation in cystic kidney diseaseR21DK088048 · NIDDK · UNIVERSITY OF KANSAS MEDICAL CENTER · PI TRAN, PAMELA VIVIAN · 2010 to 2011
$426k
NIDDK NIH HHS R01 DK084097NIDDK NIH HHS R01DK084097NIDDK NIH HHS R21 DK088048NIDDK NIH HHS R21DK088048NIGMS NIH HHS P20 GM104936NIGMS NIH HHS P20 GM104936-06
6 · The paper itself

Abstract

For more than a decade, evidence has accumulated linking dysfunction of primary cilia to renal cystogenesis, yet molecular mechanisms remain undefined. The pathogenesis of renal cysts is complex, involving multiple cellular aberrations and signaling pathways. Adding to this complexity, primary cilia exhibit multiple roles in a context-dependent manner. On renal epithelial cells, primary cilia act as mechanosensors and trigger extracellular Ca(2+) influx in response to laminar fluid flow. During mammalian development, primary cilia mediate the Hedgehog (Hh), Wnt, and Notch pathways, which control cell proliferation and differentiation, and tissue morphogenesis. Further, experimental evidence suggests the developmental state of the kidney strongly influences renal cystic disease. Thus, we review evidence for regulation of Ca(2+) and cAMP, key molecules in renal cystogenesis, at the primary cilium, the role of Hh, Wnt, and Notch signaling in renal cystic disease, and the interplay between these developmental pathways and Ca(2+) signaling. Indeed if these developmental pathways influence renal cystogenesis, these may represent novel therapeutic targets that can be integrated into a combination therapy for renal cystic disease.

Indexed as

AnimalsCalciumCell DifferentiationCell ProliferationCiliaCyclic AMPDisease Models, AnimalHedgehog ProteinsHumansKidneyPolycystic Kidney, Autosomal DominantReceptors, NotchWnt Signaling PathwayCalciumCyclic AMPHedgehog ProteinsReceptors, Notchciliacystogenesisrenal cystssignaling

Identifiers

PMID24861210
PMCPMC4312585
OpenAlexW1945848687

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.