Evidence map›Paper›PMID 28849300›Full record

ArticlePflugers Archiv : European journal of physiology2017

TRPC6 channels modulate the response of pancreatic stellate cells to hypoxia.

Nikolaj Nielsen, Kateryna Kondratska, Tobias Ruck, Benedikt Hild, Ilya Kovalenko, Sandra Schimmelpfennig, Jana Welzig, Sarah Sargin, Otto Lindemann, Sven Christian and 3 more

Abstract read
PubMed Publisher
In one paragraph

Article in Pflugers Archiv : European journal of physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing 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

24 citing papers in PubMed, 43 citations in OpenAlex.

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  9. CaInternational journal of molecular sciences · 2022
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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

13 authors at 4 institutions in 2 countries.

Nikolaj NielsenInstitute of Physiology II, Westfälische Wilhelms-Universität Münster, Robert-Koch-Str. 27b, 48149, Münster, Germany.
Kateryna KondratskaInserm, U-1003, Equipe labellisée par la Ligue Nationale Contre le Cancer, Laboratory of Excellence, Ion Channels Science and Therapeutics, Université Lille 1, Villeneuve-d'Ascq, France.
Tobias RuckDepartment of Neurology, Albert-Schweitzer-Campus 1, Building A10, Westfälische Wilhelms-Universität Münster, 48149, Münster, Germany.
Benedikt HildInstitute of Physiology II, Westfälische Wilhelms-Universität Münster, Robert-Koch-Str. 27b, 48149, Münster, Germany.
Ilya KovalenkoBayer-Pharma AG, Müllerstr. 178, 13353, Berlin, Germany.
Sandra SchimmelpfennigInstitute of Physiology II, Westfälische Wilhelms-Universität Münster, Robert-Koch-Str. 27b, 48149, Münster, Germany.
Jana WelzigInstitute of Physiology II, Westfälische Wilhelms-Universität Münster, Robert-Koch-Str. 27b, 48149, Münster, Germany.
Sarah SarginInstitute of Physiology II, Westfälische Wilhelms-Universität Münster, Robert-Koch-Str. 27b, 48149, Münster, Germany.
Otto LindemannInstitute of Physiology II, Westfälische Wilhelms-Universität Münster, Robert-Koch-Str. 27b, 48149, Münster, Germany.
Sven ChristianBayer-Pharma AG, Müllerstr. 178, 13353, Berlin, Germany.
Sven G MeuthDepartment of Neurology, Albert-Schweitzer-Campus 1, Building A10, Westfälische Wilhelms-Universität Münster, 48149, Münster, Germany.
Natalia PrevarskayaInserm, U-1003, Equipe labellisée par la Ligue Nationale Contre le Cancer, Laboratory of Excellence, Ion Channels Science and Therapeutics, Université Lille 1, Villeneuve-d'Ascq, France.
Albrecht SchwabInstitute of Physiology II, Westfälische Wilhelms-Universität Münster, Robert-Koch-Str. 27b, 48149, Münster, Germany. aschwab@uni-muenster.de.
University of Münster · DEBayer (Germany) · DEInserm · FRLa Ligue Contre le Cancer · FR

Funding

Deutsche Forschungsgemeinschaft SCHW 407/17-1Deutsche Forschungsgemeinschaft, Cells-in-Motion Cluster of Excellence EXC 1003 - CiMFP7 People: Marie-Curie Actions 289648
6 · The paper itself

Abstract

Pancreatic cancer is characterized by a massive fibrosis (desmoplasia), which is primarily caused by activated pancreatic stellate cells (PSCs). This leads to a hypoxic tumor microenvironment further reinforcing the activation of PSCs by stimulating their secretion of growth factors and chemokines. Since many of them elicit their effects via G-protein-coupled receptors (GPCRs), we tested whether TRPC6 channels, effector proteins of many G-protein-coupled receptor pathways, are required for the hypoxic activation of PSCs. Thus far, the function of ion channels in PSCs is virtually unexplored. qPCR revealed TRPC6 channels to be one of the most abundant TRPC channels in primary cultures of murine PSCs. TRPC6 channel function was assessed by comparing PSCs from TRPC6

Indexed as

AnimalsCell HypoxiaCells, CulturedFemaleMaleMiceMice, KnockoutPancreatic NeoplasmsPancreatic Stellate CellsTRPC6 Cation ChannelTRPC Cation ChannelsTumor MicroenvironmentTRPC6 Cation ChannelTrpc6 protein, mouseTRPC Cation ChannelsHypoxiaMigrationPancreatic stellate cellTRPC6 channelTumor microenvironment

Identifiers

PMID28849300
OpenAlexW2750238379

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.