Evidence map›Paper›PMID 23432060›Full record

ReviewCurrent topics in medicinal chemistry2013

Transient receptor potential (TRP) channels and cardiac fibrosis.

Zhichao Yue, Yanhui Zhang, Jia Xie, Jianmin Jiang, Lixia Yue

Open access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Current topics in medicinal chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
6.9field-weighted citation impact, top 2% 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

44 citing papers in PubMed, 83 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. The Dysfunction of CaInternational journal of molecular sciences · 2023
    Review
  6. Role of TRP Channels in Liver-Related Diseases.International journal of molecular sciences · 2023
    Review
  7. Article
  8. Hydrogel cultures reveal Transient Receptor Potential Vanilloid 4 regulation of myofibroblast activation and proliferation in valvular interstitial cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
    Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. TRPM4 non-selective cation channel in human atrial fibroblast growth.Pflugers Archiv : European journal of physiology · 2020
    Article
  16. Article
  17. The Roles of Noncardiomyocytes in Cardiac Remodeling.International journal of biological sciences · 2020
    Review
  18. Article
  19. Review
  20. 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

5 authors at 1 institution in 1 country.

Zhichao YueCalhoun Cardiology Center, Department of Cell Biology, University of Connecticut Health Center, Farmington, CT 06030, USA.
Yanhui Zhang
Jia Xie
Jianmin Jiang
Lixia Yue
UConn Health · US

Funding

Ca2+ signaling mechanisms in cardiac fibrosisR01HL078960 · NHLBI · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI YUE, LIXIA · 2005 to 2015
$3.9M
NHLBI NIH HHS 2R01HL078960NHLBI NIH HHS R01 HL078960
6 · The paper itself

Abstract

Cardiac fibrosis is associated with most cardiac diseases. Fibrosis is an accumulation of excessive extracellular matrix proteins (ECM) synthesized by cardiac fibroblasts and myofibroblasts. Fibroblasts are the most prevalent cell type in the heart, comprising 75% of cardiac cells. Myofibroblasts are hardly present in healthy normal heart tissue, but appear abundantly in diseased hearts. Cardiac fibroblasts are activated by a variety of pathological stimuli, such as myocardial injury, oxidative stress, mechanical stretch, and elevated autocrine-paracrine mediators, thereby undergoing proliferation, differentiation to myofibroblasts, and production of various cytokines and ECM proteins. A number of signaling pathways and bioactive molecules are involved and work in concert to activate fibroblasts and myofibroblasts in the fibrogenesis cascade. Fibroblasts and myofibroblasts are not only principal ECM producers, but also play a central role in fibrogenesis and myocardial remodeling in fibrotic heart disease. Thus, understanding the biological processes of cardiac fibroblasts will provide novel insights into the underlying mechanisms of fibrosis and provide potential targets for developing antifibrotic drugs. Recent studies demonstrate that Ca2+ signal is essential for fibroblast proliferation, differentiation, and ECM-protein production. This review focuses on the recent advances in understanding molecular mechanisms of Ca2+ signaling in cardiac fibrogenesis, and potential role of Ca(2+)-permeable channels, in particular, the transient potential (TRP) channels in fibrotic heart disease. TRP channels are highly expressed in cardiac fibroblasts. TRPM7 has been shown to be essential in TGFβ1 mediated fibrogenesis, and TRPC3 has been demonstrated to play an essential role in regulating fibroblast function. Thus, the Ca2+-permeable TRP channels may serve as potential novel targets for developing anti-fibrotic drugs.

Indexed as

AnimalsCalciumFibrosisHeart DiseasesHumansMolecular Targeted TherapySignal TransductionTransient Receptor Potential ChannelsCalciumTransient Receptor Potential Channels

Identifiers

PMID23432060
PMCPMC3874073
OpenAlexW2015366584

What OpenQuestion holds

Textmetadata
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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.