Evidence map›Paper›PMID 27383564›Full record

ArticleScientific reports2016

TRPC6 channel activation promotes neonatal glomerular mesangial cell apoptosis via calcineurin/NFAT and FasL/Fas signaling pathways.

Hitesh Soni, Adebowale Adebiyi

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

17 citing papers in PubMed, 39 citations in OpenAlex.

  1. Non-voltage-gated CaAmerican journal of physiology. Renal physiology · 2024
    Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Renal vascular TRP channels.Current research in physiology · 2021
    Article
  8. Article
  9. Article
  10. TotalCardiovascular diagnosis and therapy · 2019
    Article
  11. Article
  12. Article
  13. Role of adaptor protein p66Shc in renal pathologies.American journal of physiology. Renal physiology · 2018
    Review
  14. Urotensin II-induced store-operated CaScientific reports · 2017
    Article
  15. Article
  16. Article
  17. 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

2 authors at 1 institution in 1 country.

Hitesh SoniDepartment of Physiology University of Tennessee Health Science Center, Memphis TN, USA.
Adebowale AdebiyiDepartment of Physiology University of Tennessee Health Science Center, Memphis TN, USA.
University of Tennessee Health Science Center · US

Funding

Regulation of neonatal renal hemodynamicsR01DK101668 · NIDDK · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI ADEBIYI, ADEBOWALE · 2014 to 2018
$1.7M
NIDDK NIH HHS R01 DK101668
6 · The paper itself

Abstract

Glomerular mesangial cell (GMC) proliferation and death are involved in the pathogenesis of glomerular disorders. The mechanisms that control GMC survival are poorly understood, but may include signal transduction pathways that are modulated by changes in intracellular Ca(2+) ([Ca(2+)]i) concentration. In this study, we investigated whether activation of the canonical transient receptor potential (TRPC) 6 channels and successive [Ca(2+)]i elevation alter neonatal GMC survival. Hyperforin (HF)-induced TRPC6 channel activation increased [Ca(2+)]i concentration, inhibited proliferation, and triggered apoptotic cell death in primary neonatal pig GMCs. HF-induced neonatal GMC apoptosis was not associated with oxidative stress. However, HF-induced TRPC6 channel activation stimulated nuclear translocation of the nuclear factor of activated T-cells, cytoplasmic 1 (NFATc1). HF also increased cell death surface receptor Fas ligand (FasL) level and caspase-8 activity in the cells; effects mitigated by [Ca(2+)]i chelator BAPTA, calcineurin/NFAT inhibitor VIVIT, and TRPC6 channel knockdown. Accordingly, HF-induced neonatal GMC apoptosis was attenuated by BAPTA, VIVIT, Fas blocking antibody, and a caspase-3/7 inhibitor. These findings suggest that TRPC6 channel-dependent [Ca(2+)]i elevation and the ensuing induction of the calcineurin/NFAT, FasL/Fas, and caspase signaling cascades promote neonatal pig GMC apoptosis.

Indexed as

AnimalsAnimals, NewbornApoptosisCalcineurinCalciumCalcium SignalingCaspase 8Caspase InhibitorsCell DivisionCells, CulturedEgtazic AcidFas Ligand Proteinfas ReceptorIon TransportMesangial CellsNFATC Transcription Factors1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acidCalcineurinCalciumCaspase 8Caspase InhibitorsEgtazic AcidFas Ligand Proteinfas ReceptorhyperforinNFATC Transcription FactorsOligopeptidesPhloroglucinolRNA, Small InterferingTerpenesTRPC6 Cation ChannelVIVIT peptide

Identifiers

PMID27383564
PMCPMC4935859
OpenAlexW2469239379

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.