Evidence map›Paper›PMID 34190686›Full record

ArticleeLife2021

The Ca

Yang Guo, Ze-Yan Yu, Jianxin Wu, Hutao Gong, Scott Kesteven, Siiri E Iismaa, Andrea Y Chan, Sara Holman, Silvia Pinto, Andy Pironet and 5 more

Open access · goldAbstract read
In one paragraph

Article in eLife, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

23 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Review
  3. Stress-Induced calcium mishandling in cardiac (Patho)physiology.Cellular and molecular life sciences : CMLS · 2025
    Review
  4. Novel Drug Targets in Diastolic Heart Disease.International journal of molecular sciences · 2025
    Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. The Role of TRPM4 in Cardiac Electrophysiology and Arrhythmogenesis.International journal of molecular sciences · 2023
    Review
  13. Ion Channels in the Development and Remodeling of the Aortic Valve.International journal of molecular sciences · 2023
    Review
  14. Mild allergic airways responses to an environmental mixture increase cardiovascular risk in rats.Toxicological sciences : an official journal of the Society of Toxicology · 2023
    Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article
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

15 authors at 2 institutions in 2 countries.

Yang Guo *Molecular Cardiology and Biophysics Division, Victor Chang Cardiac Research Institute, Sydney, Australia.
Ze-Yan Yu *Molecular Cardiology and Biophysics Division, Victor Chang Cardiac Research Institute, Sydney, Australia.
Jianxin WuMolecular Cardiology and Biophysics Division, Victor Chang Cardiac Research Institute, Sydney, Australia.
Hutao GongCardiac Physiology and Transplantation Division, Victor Chang Cardiac Research Institute, Sydney, Australia.
Scott KestevenCardiac Physiology and Transplantation Division, Victor Chang Cardiac Research Institute, Sydney, Australia.
Siiri E IismaaMolecular Cardiology and Biophysics Division, Victor Chang Cardiac Research Institute, Sydney, Australia.
Andrea Y ChanMolecular Cardiology and Biophysics Division, Victor Chang Cardiac Research Institute, Sydney, Australia.
Sara HolmanMolecular Cardiology and Biophysics Division, Victor Chang Cardiac Research Institute, Sydney, Australia.
Silvia PintoLaboratory of Ion Channel Research, Department of Molecular and Cellular Medicine, Katholieke Universiteit Leuven, Leuven, Belgium.
Andy PironetLaboratory of Ion Channel Research, Department of Molecular and Cellular Medicine, Katholieke Universiteit Leuven, Leuven, Belgium.
Charles D CoxMolecular Cardiology and Biophysics Division, Victor Chang Cardiac Research Institute, Sydney, Australia.
Robert M GrahamMolecular Cardiology and Biophysics Division, Victor Chang Cardiac Research Institute, Sydney, Australia.
Rudi VennekensLaboratory of Ion Channel Research, Department of Molecular and Cellular Medicine, Katholieke Universiteit Leuven, Leuven, Belgium.
Michael P FeneleyCardiac Physiology and Transplantation Division, Victor Chang Cardiac Research Institute, Sydney, Australia.
Boris MartinacMolecular Cardiology and Biophysics Division, Victor Chang Cardiac Research Institute, Sydney, Australia.ORCID 0000-0001-8422-7082
Victor Chang Cardiac Research Institute · AUKU Leuven · BE

Funding

Fonds Wetenschappelijk Onderzoek G0E0317NKU Leuven TRPLeNational Health and Medical Research Council APP1108013National Health and Medical Research Council APP1135974NSW Health EMCRFellowship
6 · The paper itself

Abstract

Pathological left ventricular hypertrophy (LVH) occurs in response to pressure overload and remains the single most important clinical predictor of cardiac mortality. The molecular pathways in the induction of pressure overload LVH are potential targets for therapeutic intervention. Current treatments aim to remove the pressure overload stimulus for LVH, but do not completely reverse adverse cardiac remodelling. Although numerous molecular signalling steps in the induction of LVH have been identified, the initial step by which mechanical stretch associated with cardiac pressure overload is converted into a chemical signal that initiates hypertrophic signalling remains unresolved. In this study, we show that selective deletion of transient receptor potential melastatin 4 (TRPM4) channels in mouse cardiomyocytes results in an approximately 50% reduction in the LVH induced by transverse aortic constriction. Our results suggest that TRPM4 channel is an important component of the mechanosensory signalling pathway that induces LVH in response to pressure overload and represents a potential novel therapeutic target for the prevention of pathological LVH.

Indexed as

Gene DeletionAnimalsHypertrophy, Left VentricularMaleMiceMice, Inbred C57BLMyocytes, CardiacSignal TransductionTRPM Cation ChannelsTRPM4 protein, mouseTRPM Cation ChannelsCa2+/calmodulin-dependent protein kinase IIcardiovascular diseasecell biologyleft ventricular hypertrophymechanosensitive channelsmedicinemouse

Identifiers

PMID34190686
PMCPMC8245133
OpenAlexW3173620075

What Socratic 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 Socratic graph.