Evidence map›Paper›PMID 26490951›Full record

ReviewPediatric nephrology (Berlin, Germany)2016

Calcium, TRPC channels, and regulation of the actin cytoskeleton in podocytes: towards a future of targeted therapies.

Nicolas Wieder, Anna Greka

Open access · hybridAbstract readCase ReportsReview
In one paragraph

Review in Pediatric nephrology (Berlin, Germany), 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
3.1field-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

30 citing papers in PubMed, 52 citations in OpenAlex.

  1. Review
  2. Article
  3. The Life of a Kidney Podocyte.Acta physiologica (Oxford, England) · 2025
    Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Molecular pathways that drive diabetic kidney disease.The Journal of clinical investigation · 2023
    Review
  9. Histone modification in podocyte injury of diabetic nephropathy.Journal of molecular medicine (Berlin, Germany) · 2022
    Review
  10. Article
  11. Review
  12. Article
  13. Cytoskeleton Rearrangements Modulate TRPC6 Channel Activity in Podocytes.International journal of molecular sciences · 2021
    Article
  14. Renal vascular TRP channels.Current research in physiology · 2021
    Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. 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

2 authors at 1 institution in 1 country.

Nicolas WiederRenal Division, Department of Medicine and Glom-NExT Center for Glomerular Kidney Disease and Novel Experimental Therapeutics, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
Anna GrekaRenal Division, Department of Medicine and Glom-NExT Center for Glomerular Kidney Disease and Novel Experimental Therapeutics, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA. agreka@bwh.harvard.edu.
Harvard University · US

Funding

Molecular mechanisms of podocyte injury in FSGSR01DK095045 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI Anna Greka, Juan Lorenzo Pablo · 2014 to 2026
$5.1M
Role of TRPC5 channel inhibition in the treatment of glomerular diseaseR01DK099465 · NIDDK · BROAD INSTITUTE, INC. · PI Anna Greka · 2014 to 2026
$5.1M
NIDDK NIH HHS R01 DK095045NIDDK NIH HHS R01 DK099465
6 · The paper itself

Abstract

With more than 6,000 new pediatric patients with treatment-resistant nephrotic syndrome in the US each year alone, the unmet need for novel, podocyte-specific therapies is substantial. Recently, the established therapeutic benefit of angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARB) was used as a starting point to gain insight into the pathomechanism of primary podocytopathies. A calcium (Ca(2+))-mediated pathway has been identified that connects the angiotensin type 1 receptor (AT1R) to podocyte cytoskeletal dynamics, essential for a functioning glomerular filtration barrier. This discovery provided an important missing piece in our understanding of the pathomechanism of filter barrier damage, revealing Ca(2+) signaling as critical for podocyte health and disease. The identification of the two Ca(2+) permeant channels TRPC5 and TRPC6 as mediators of this pathway not only bolstered the importance of podocyte cytoskeleton dynamics but also revealed promising drug targets for treatment-resistant nephrotic syndrome. This review will focus on this novel signaling pathway in primary podocytopathies and its implications for next-generation therapies for glomerular disease.

Indexed as

Actin CytoskeletonAdolescentAnimalsCalciumChildHumansMaleMolecular Targeted TherapyNephrotic SyndromePodocytesTRPC Cation ChannelsCalciumTRPC Cation ChannelsAngiotensin type 1 receptor (ATR1)CalciumChildrenCytoskeletonGlomerular diseasePodocytopathiesSteroid-resistant nephrotic syndromeTRPC channels

Identifiers

PMID26490951
PMCPMC4840088
OpenAlexW2180226417

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.