Evidence map›Paper›PMID 26084930›Full record

ReviewAmerican journal of physiology. Renal physiology2015

TRPC6 channel as an emerging determinant of the podocyte injury susceptibility in kidney diseases.

Daria V Ilatovskaya, Alexander Staruschenko

Abstract readReview
In one paragraph

Review in American journal of physiology. Renal physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

79 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Review
  6. TRPC6-Mediated CaCells · 2026
    Article
  7. Review
  8. Article
  9. Review
  10. Wnt/β-Catenin Signaling in Diabetic Complications: Mechanisms and Therapeutic Potential.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026
    Review
  11. Genotype-phenotype correlations and clinical outcomes of genetic TRPC6 podocytopathies.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2025
    Observational
  12. Review
  13. Article
  14. The CaPediatric nephrology (Berlin, Germany) · 2025
    Review
  15. Article
  16. PIEZO1-Mediated Calcium Signaling and Podocyte Injury in Diabetic Kidney Disease.Journal of the American Society of Nephrology : JASN · 2025
    Article
  17. Review
  18. Non-voltage-gated CaAmerican journal of physiology. Renal physiology · 2024
    Review
  19. Review
  20. Cytoskeleton Rearrangement in Podocytopathies: An Update.International journal of molecular sciences · 2024
    Review

19 more citing papers are in PubMed but not listed here.

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

2 authors.

Daria V IlatovskayaDepartment of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin; and dilatovskaya@mcw.edu.
Alexander StaruschenkoDepartment of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin; and Cardiovascular Center, Medical College of Wisconsin, Milwaukee, Wisconsin.ORCID http://orcid.org/0000-0002-5190-8356

Funding

Mechanisms and relevance of ENaC regulation by EGF and Rac1R01HL108880 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI STARUSCHENKO, ALEXANDER · 2012 to 2016
$1.9M
Role of NOX4 In Kidney Function In Salt-Sensitive HypertensionR01HL122662 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI COWLEY, ALLEN W, STARUSCHENKO, ALEXANDER · 2015 to 2018
$1.5M
NHLBI NIH HHS R01 HL108880NHLBI NIH HHS R01 HL122662
6 · The paper itself

Abstract

Podocytes (terminally differentiated epithelial cells of the glomeruli) play a key role in the maintenance of glomerular structure and permeability and in the incipiency of various renal abnormalities. Injury to podocytes is considered a major contributor to the development of kidney disease as their loss causes proteinuria and progressive glomerulosclerosis. The physiological function of podocytes is critically dependent on proper intracellular calcium handling; excessive calcium influx in these cells may result in the effacement of foot processes, apoptosis, and subsequent glomeruli damage. One of the key proteins responsible for calcium flux in the podocytes is transient receptor potential cation channel, subfamily C, member 6 (TRPC6); a gain-of-function mutation in TRPC6 has been associated with the onset of the familial forms of focal segmental glomerulosclerosis (FSGS). Recent data also revealed a critical role of this channel in the onset of diabetic nephropathy. Therefore, major efforts of the research community have been recently dedicated to unraveling the TRPC6-dependent effects in the initiation of podocyte injury. This mini-review focuses on the TRPC6 channel in podocytes and colligates recent data in an attempt to shed some light on the mechanisms underlying the pathogenesis of TRPC6-mediated glomeruli damage and its potential role as a therapeutic target for the treatment of chronic kidney diseases.

Indexed as

Diabetic NephropathiesDisease SusceptibilityGlomerulosclerosis, Focal SegmentalHumansKidney DiseasesMutationPodocytesSignal TransductionTRPC6 Cation ChannelTRPC Cation ChannelsTRPC6 Cation ChannelTRPC6 protein, humanTRPC Cation Channelsdiabetic nephropathyglomerulosclerosisglomerulusintracellular calciumpodocyteproteinuriaTRPC6

Identifiers

PMID26084930
PMCPMC4556891

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.