Evidence map›Paper›PMID 26656101›Full record

ArticleScientific reports2015

Podocyte injury in diabetic nephropathy: implications of angiotensin II-dependent activation of TRPC channels.

Daria V Ilatovskaya, Vladislav Levchenko, Andrea Lowing, Leonid S Shuyskiy, Oleg Palygin, Alexander Staruschenko

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
6.8field-weighted citation impact, top 2% 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

66 citing papers in PubMed, 108 citations in OpenAlex.

  1. Article
  2. Review
  3. Blood Pressure Management Strategies and Podocyte Health.American journal of hypertension · 2025
    Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Renin-angiotensin system-mediated nitric oxide signaling in podocytes.American journal of physiology. Renal physiology · 2024
    Article
  9. Calcium signalling and transport in the kidney.Nature reviews. Nephrology · 2024
    Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. A Putative Role for TRPC6 in Immune-Mediated Kidney Injury.International journal of molecular sciences · 2023
    Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Review

6 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

6 authors at 1 institution in 2 countries.

Daria V IlatovskayaDepartment of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin 53226, USA.
Vladislav LevchenkoDepartment of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin 53226, USA.
Andrea LowingDepartment of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin 53226, USA.
Leonid S ShuyskiyDepartment of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin 53226, USA.
Oleg PalyginDepartment of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin 53226, USA.
Alexander StaruschenkoDepartment of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin 53226, USA.
Medical College of Wisconsin · US

Funding

INTEGRATED PHYSIOLOGY TRAINING--MOLECULE TO ORGANISMT32HL007852 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI Matthew Robert Hodges · 1996 to 2026
$6.5M
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
The involvement of ATP-dependent inhibition of ENaC in ARPKD cystogenesisR00DK105160 · NIDDK · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI ILATOVSKAYA, DARIA · 2018 to 2020
$747k
The involvement of ATP-dependent inhibition of ENaC in ARPKD cystogenesisK99DK105160 · NIDDK · MEDICAL COLLEGE OF WISCONSIN · PI ILATOVSKAYA, DARIA · 2015 to 2016
$180k
NHLBI NIH HHS R01 HL108880NHLBI NIH HHS R01 HL122662NHLBI NIH HHS T32 HL007852NIDDK NIH HHS K99 DK105160NIDDK NIH HHS R00 DK105160
6 · The paper itself

Abstract

Injury to podocytes is considered a major contributor to diabetic kidney disease: their loss causes proteinuria and progressive glomerulosclerosis. Podocyte depletion may result from improper calcium handling due to abnormal activation of the calcium permeant TRPC (Transient Receptor Potential Canonical) channels. Angiotensin II (Ang II) levels are found to be elevated in diabetes; furthermore, it was reported that Ang II causes activation of TRPC6 in podocytes. We hypothesized here that Ang II-mediated calcium influx is aggravated in the podocytes under the conditions of type 1 diabetic nephropathy (DN). Diabetes was induced in the Dahl Salt-Sensitive rats by an injection of streptozotocin (STZ-SS). Eleven weeks post treatment was sufficient for the animals to develop hyperglycemia, excessive urination, weight loss, microalbuminuria, nephrinuria and display renal histological lesions typical for patients with DN. Patch-clamp electrophysiology performed on podocytes of the freshly isolated glomeruli showed enhanced basal TRPC channel activity in the STZ-SS rats, and increased response to Ang II; total calcium influx triggered by Ang II application was also augmented in podocytes of these rats. Our studies have a strong potential for advancing the understanding of TRPC-mediated effects on podocytopenia in DN initiation.

Indexed as

AlbuminuriaAngiotensin IIAnimalsCalciumDiabetic NephropathiesDisease Models, AnimalGene ExpressionPodocytesRatsRats, Inbred DahlTRPC Cation ChannelsAngiotensin IICalciumTrpc6 protein, ratTRPC Cation Channels

Identifiers

PMID26656101
PMCPMC4674698
OpenAlexW2415143293

What OpenQuestion holds

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Registered trials

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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.