Evidence map›Paper›PMID 29532428›Full record

ArticleJournal of cardiovascular translational research2018

TRPC1 Deficiency Impairs the Endothelial Progenitor Cell Function via Inhibition of Calmodulin/eNOS Pathway.

Lai-Ling Du, Zhida Shen, Zhengwei Li, Xuewei Ye, Meiping Wu, Lihui Hong, Yanbo Zhao

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of cardiovascular translational research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.4field-weighted citation impact, top 24% 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

14 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Role of TRP Channels in Liver-Related Diseases.International journal of molecular sciences · 2023
    Review
  3. Article
  4. Transient Receptor Potential (TRP) Channels in Tumor Vascularization.International journal of molecular sciences · 2022
    Review
  5. Article
  6. New Insights into TRP Ion Channels in Stem Cells.International journal of molecular sciences · 2022
    Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Endothelial CaInternational journal of molecular sciences · 2019
    Review
  12. Review
  13. Article
  14. 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

7 authors at 3 institutions in 1 country.

Lai-Ling DuSchool of Health and Social Management, Zhejiang Shuren University, Hangzhou, Zhejiang, 310015, China. dulailing@163.com.
Zhida ShenDepartment of Cardiology, Sir Run Run Shaw Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang, 310016, China.
Zhengwei LiDepartment of Cardiology, Sir Run Run Shaw Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang, 310016, China.
Xuewei YeSchool of Health and Social Management, Zhejiang Shuren University, Hangzhou, Zhejiang, 310015, China.
Meiping WuSchool of Health and Social Management, Zhejiang Shuren University, Hangzhou, Zhejiang, 310015, China.
Lihui HongSchool of Health and Social Management, Zhejiang Shuren University, Hangzhou, Zhejiang, 310015, China.
Yanbo ZhaoDepartment of Cardiology, Sir Run Run Shaw Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang, 310016, China. zhaoybzju@zju.edu.cn.
Zhejiang Shuren University · CNZhejiang University · CNSir Run Run Shaw Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endothelial progenitor cells (EPCs) promote angiogenesis and play a pivotal role in endothelial repair and re-endothelialization after vascular injury. Transient receptor potential-canonical1 (TRPC1) has been recently implied to play important roles on EPC function. Here, we studied the role of TRPC1 in regulating EPC function in vivo and in vitro. EPCs were cultured from TRPC1-knockout mice and their controls. In vitro, TRPC1 knockout reduced EPC functional activities, including migration and tube formation. Additionally, calmodulin (CaM)/endothelial nitric oxide synthase (eNOS) signaling activity were downregulated after TRPC1 knockout. Administration of CaM or eNOS inhibitor ameliorated TRPC1 knockout-reduced EPC migration and tube formation. In vivo Matrigel plug assay confirmed that TRPC1 knockout decreased formation of functional blood vessels of EPCs compared with wild-type EPCs. Taken together, these data suggest that TRPC1 is a critical regulator of angiogenesis.

Indexed as

AnimalsBlotting, WesternCalmodulinCell MovementCell ProliferationCells, CulturedDisease Models, AnimalEndothelial Progenitor CellsMaleMiceNeovascularization, PathologicNitric Oxide Synthase Type IIISignal TransductionTRPC Cation ChannelsVascular System InjuriesCalmodulinNitric Oxide Synthase Type IIINos3 protein, mousetransient receptor potential cation channel, subfamily C, member 1TRPC Cation ChannelsCalmodulinEndothelial progenitor cellseNOSTRPC1

Identifiers

PMID29532428
OpenAlexW2792567835

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.