Evidence map›Paper›PMID 32219126›Full record

ArticleBioMed research international2020

Transient Receptor Potential Channel Canonical Type 3 Deficiency Antagonizes Myofibroblast Transdifferentiation In Vivo.

Weijie Xia, Qianran Wang, Yuangang Lu, Yingru Hu, Xingcun Zhang, Junbo Zhang, Dongfang Liu, Jinlin Song, Zhiming Zhu, Daoyan Liu and 1 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BioMed research international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.4field-weighted citation impact, top 42% 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

2 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. 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

11 authors at 4 institutions in 1 country.

Weijie XiaDepartment of Burn & Plastic Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.ORCID https://orcid.org/0000-0003-1065-7121
Qianran WangDepartment of Endocrinology, The Second Affiliated Hospital, Chongqing Medical University, Chongqing 400010, China.ORCID https://orcid.org/0000-0003-0098-839X
Yuangang LuDepartment of Plastic & Cosmetic Surgery, Research Institute of Surgery, Daping Hospital, Third Military Medical University, Chongqing 400042, China.
Yingru HuDepartment of Hypertension and Endocrinology, Center for Hypertension and Metabolic Diseases, Daping Hospital, Third Military Medical University, Chongqing Institute of Hypertension, Chongqing 400042, China.
Xingcun ZhangDepartment of Plastic & Cosmetic Surgery, Research Institute of Surgery, Daping Hospital, Third Military Medical University, Chongqing 400042, China.
Junbo ZhangDepartment of Plastic & Cosmetic Surgery, Research Institute of Surgery, Daping Hospital, Third Military Medical University, Chongqing 400042, China.
Dongfang LiuDepartment of Endocrinology, The Second Affiliated Hospital, Chongqing Medical University, Chongqing 400010, China.
Jinlin SongSchool of Dental Medicine, Chongqing Medical University, Chongqing 400016, China.
Zhiming ZhuDepartment of Hypertension and Endocrinology, Center for Hypertension and Metabolic Diseases, Daping Hospital, Third Military Medical University, Chongqing Institute of Hypertension, Chongqing 400042, China.
Daoyan LiuDepartment of Hypertension and Endocrinology, Center for Hypertension and Metabolic Diseases, Daping Hospital, Third Military Medical University, Chongqing Institute of Hypertension, Chongqing 400042, China.ORCID https://orcid.org/0000-0002-8708-9137
Hengshu ZhangDepartment of Burn & Plastic Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.ORCID https://orcid.org/0000-0003-0942-4881
Army Medical University · CNThe Affiliated Yongchuan Hospital of Chongqing Medical University · CNChongqing Medical University · CNDalian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveMyofibroblast transformation has been shown to be associated with the reactive oxygen species- (ROS-) producing enzyme NADPH oxidase (Nox4). Inhibition of transient receptor potential channel canonical type 3 (TRPC3) attenuates mitochondrial calcium handling and ROS production in the vasculature of hypertensive rats. However, it remains elusive whether TRPC3 regulates mitochondrial calcium and ROS production and participates in myofibroblast transdifferentiation during wound healing. METHODS AND

resultsIn this study, we demonstrated that activation of TRPC3 by transforming growth factor

conclusionsOur data indicate that TGF

Indexed as

ActinsAdultAnimalsCalciumCell TransdifferentiationFemaleHumansMaleMiceMice, KnockoutMiddle AgedMitochondriaMyofibroblastsPyrazolesReactive Oxygen SpeciesTransforming Growth Factor betaActinsalpha-smooth muscle actin, mouseCalciumethyl-1-(4-(2*3*3-trichloroacrylamide)phenyl)-5-(trifluoromethyl)-1H-pyrazole-4-carboxylatePyrazolesReactive Oxygen SpeciesTransforming Growth Factor betaTRPC3 cation channelTRPC Cation Channels

Identifiers

PMID32219126
PMCPMC7077044
OpenAlexW3009847683

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.