Evidence map›Paper›PMID 22918967›Full record

ArticleMolecular pharmacology2012

Coordinated regulation of murine cardiomyocyte contractility by nanomolar (-)-epigallocatechin-3-gallate, the major green tea catechin.

Wei Feng, Hyun Seok Hwang, Dmytro O Kryshtal, Tao Yang, Isela T Padilla, Asheesh K Tiwary, Birgit Puschner, Isaac N Pessah, Björn C Knollmann

Open access · bronzeAbstract read
In one paragraph

Article in Molecular pharmacology, 2012. 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
1.0field-weighted citation impact, top 23% 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, 33 citations in OpenAlex.

  1. Review
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  8. Synergistic FRET assays for drug discovery targeting RyR2 channels.Journal of molecular and cellular cardiology · 2022
    Article
  9. Review
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  13. Hypertrophic cardiomyopathy mutations increase myofilament CaThe Journal of biological chemistry · 2018
    Article
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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

9 authors at 2 institutions in 1 country.

Wei FengDepartment of Molecular Biosciences, University of California, Davis, California, USA.
Hyun Seok Hwang
Dmytro O Kryshtal
Tao Yang
Isela T Padilla
Asheesh K Tiwary
Birgit Puschner
Isaac N Pessah
Björn C Knollmann
University of California, Davis · USVanderbilt University · US

Funding

Workshop on Environmental Technology Transfer and EntrepreneurshipP42ES004699 · NIEHS · UNIVERSITY OF CALIFORNIA DAVIS · PI HAMMOCK, BRUCE D · 1987 to 2021
$50.1M
Troponin T mutations and Sudden Cardiac DeathR01HL071670 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI KNOLLMANN, BJORN C · 2003 to 2017
$4.5M
Calsequestrin in Ventricular Arrhythmia and Sudden DeathR01HL088635 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI KNOLLMANN, BJORN C · 2007 to 2015
$3.2M
NHLBI NIH HHS HL71670NHLBI NIH HHS HL88635NHLBI NIH HHS R01 HL071670NHLBI NIH HHS R01 HL088635NIEHS NIH HHS ES04699NIEHS NIH HHS P42 ES004699
6 · The paper itself

Abstract

Green tea polyphenolic catechins exhibit biological activity in a wide variety of cell types. Although reports in the lay and scientific literature suggest therapeutic potential for improving cardiovascular health, the underlying molecular mechanisms of action remain unclear. Previous studies have implicated a wide range of molecular targets in cardiac muscle for the major green tea catechin, (-)-epigallocatechin-3-gallate (EGCG), but effects were observed only at micromolar concentrations of unclear clinical relevance. Here, we report that nanomolar concentrations of EGCG significantly enhance contractility of intact murine myocytes by increasing electrically evoked Ca(2+) transients, sarcoplasmic reticulum (SR) Ca(2+) content, and ryanodine receptor type 2 (RyR2) channel open probability. Voltage-clamp experiments demonstrate that 10 nM EGCG significantly inhibits the Na(+)-Ca(2+) exchanger. Of importance, other Na(+) and Ca(2+) handling proteins such as Ca(2+)-ATPase, Na(+)-H(+) exchanger, and Na(+)-K(+)-ATPase were not affected by EGCG ≤ 1 μM. Thus, nanomolar EGCG increases contractility in intact myocytes by coordinately modulating SR Ca(2+) loading, RyR2-mediated Ca(2+) release, and Na(+)-Ca(2+) exchange. Inhibition of Na(+)-K(+)-ATPase activity probably contributes to the positive inotropic effects observed at EGCG concentrations >1 μM. These newly recognized actions of nanomolar and micromolar EGCG should be considered when the therapeutic and toxicological potential of green tea supplementation is evaluated and may provide a novel therapeutic strategy for improving contractile function in heart failure.

Indexed as

AnimalsBiological TransportCalciumCatechinCell MembraneCell SizeIn Vitro TechniquesMiceMice, Inbred C57BLMyocardial ContractionMyocytes, CardiacRabbitsRyanodine Receptor Calcium Release ChannelSarcoplasmic ReticulumSarcoplasmic Reticulum Calcium-Transporting ATPasesSodium-Calcium ExchangerCalciumCatechinepigallocatechin gallateRyanodine Receptor Calcium Release ChannelSarcoplasmic Reticulum Calcium-Transporting ATPasesSodium-Calcium ExchangerSodium-Hydrogen ExchangersSodium-Potassium-Exchanging ATPaseTea

Identifiers

PMID22918967
PMCPMC3477230
OpenAlexW2118151068

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.