Evidence map›Paper›PMID 26788466›Full record

ReviewWorld journal of nephrology2016

Role of calcium in polycystic kidney disease: From signaling to pathology.

Alessandra Mangolini, Lucia de Stephanis, Gianluca Aguiari

Open access · hybridAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in World journal of nephrology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
4.5field-weighted citation impact, top 6% 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

30 citing papers in PubMed, 44 citations in OpenAlex.

  1. PKD2-like proteins targetProceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Plasma proteome fingerprint in kidney diseases.Frontiers in molecular biosciences · 2024
    Article
  10. Article
  11. Review
  12. The Mitochondrial CaCell calcium · 2022
    Article
  13. Review
  14. Article
  15. Inward CaAmerican journal of physiology. Renal physiology · 2021
    Article
  16. Review
  17. Review
  18. Review
  19. Targeting E3 Ubiquitin Ligases and Deubiquitinases in Ciliopathy and Cancer.International journal of molecular sciences · 2020
    Review
  20. Article
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

3 authors at 1 institution in 2 countries.

Alessandra MangoliniAlessandra Mangolini, Lucia de Stephanis, Gianluca Aguiari, Department of Biomedical and Surgical Specialty Sciences, Section of Biochemistry, Molecular Biology and Medical Genetics, University of Ferrara, 44121 Ferrara, Italy.
Lucia de StephanisAlessandra Mangolini, Lucia de Stephanis, Gianluca Aguiari, Department of Biomedical and Surgical Specialty Sciences, Section of Biochemistry, Molecular Biology and Medical Genetics, University of Ferrara, 44121 Ferrara, Italy.
Gianluca AguiariAlessandra Mangolini, Lucia de Stephanis, Gianluca Aguiari, Department of Biomedical and Surgical Specialty Sciences, Section of Biochemistry, Molecular Biology and Medical Genetics, University of Ferrara, 44121 Ferrara, Italy.
Creative Research Enterprises (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autosomal dominant polycystic kidney disease (ADPKD) is the most common inherited monogenic kidney disease. Characterized by the development and growth of cysts that cause progressive kidney enlargement, it ultimately leads to end-stage renal disease. Approximately 85% of ADPKD cases are caused by mutations in the PKD1 gene, while mutations in the PKD2 gene account for the remaining 15% of cases. The PKD1 gene encodes for polycystin-1 (PC1), a large multi-functional membrane receptor protein able to regulate ion channel complexes, whereas polycystin-2 (PC2), encoded by the PKD2 gene, is an integral membrane protein that functions as a calcium-permeable cation channel, located mainly in the endoplasmic reticulum (ER). In the primary cilia of the epithelial cells, PC1 interacts with PC2 to form a polycystin complex that acts as a mechanosensor, regulating signaling pathways involved in the differentiation of kidney tubular epithelial cells. Despite progress in understanding the function of these proteins, the molecular mechanisms associated with the pathogenesis of ADPKD remain unclear. In this review we discuss how an imbalance between functional PC1 and PC2 proteins may disrupt calcium channel activities in the cilium, plasma membrane and ER, thereby altering intracellular calcium signaling and leading to the aberrant cell proliferation and apoptosis associated with the development and growth of renal cysts. Research in this field could lead to the discovery of new molecules able to rebalance intracellular calcium, thereby normalizing cell proliferation and reducing kidney cyst progression.

Indexed as

Autosomal dominant polycystic kidney diseaseCalcium signalingcAMPCell growthNon-capacitative calcium entry

Identifiers

PMID26788466
PMCPMC4707171
OpenAlexW2418240946

What OpenQuestion holds

Textmetadata
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.