Evidence map›Paper›PMID 24447627›Full record

ArticleLife sciences2014

Alpha1 catalytic subunit of AMPK modulates contractile function of cardiomyocytes through phosphorylation of troponin I.

Si Chen, Ping Zhu, Hui-Ming Guo, Raquel Sancho Solis, Yanqing Wang, Yina Ma, Jinli Wang, Junjie Gao, Ji-Mei Chen, Ying Ge and 2 more

Open access · greenAbstract read
In one paragraph

Article in Life sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

18 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Article
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  7. Pim-1 Kinase Phosphorylates Cardiac Troponin I and Regulates Cardiac Myofilament Function.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2018
    Article
  8. L-Carnitine Attenuates Cardiac Dysfunction by Ischemic Insults Through Akt Signaling Pathway.Toxicological sciences : an official journal of the Society of Toxicology · 2017
    Article
  9. Article
  10. Article
  11. Article
  12. Article
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  14. Article
  15. The Modulation of Cardiac Contractile Function by the Pharmacological and Toxicological Effects of Urocortin2.Toxicological sciences : an official journal of the Society of Toxicology · 2015
    Article
  16. Article
  17. Sestrin2 promotes LKB1-mediated AMPK activation in the ischemic heart.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015
    Article
  18. 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

12 authors at 3 institutions in 2 countries.

Si ChenDepartment of Pharmacology and Toxicology, School of Medicine and Biomedical Sciences, University at Buffalo - State University of New York, Buffalo, NY, United States.
Ping ZhuDepartment of Cardiovascular Surgery, Guangdong Cardiovascular Institute, Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China.
Hui-Ming GuoDepartment of Cardiovascular Surgery, Guangdong Cardiovascular Institute, Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China.
Raquel Sancho SolisDepartment of Cell and Regenerative Biology, School of Medicine and Public Health, University of Wisconsin - Madison, WI, United States.
Yanqing WangDepartment of Pharmacology and Toxicology, School of Medicine and Biomedical Sciences, University at Buffalo - State University of New York, Buffalo, NY, United States.
Yina MaDepartment of Pharmacology and Toxicology, School of Medicine and Biomedical Sciences, University at Buffalo - State University of New York, Buffalo, NY, United States.
Jinli WangDepartment of Pharmacology and Toxicology, School of Medicine and Biomedical Sciences, University at Buffalo - State University of New York, Buffalo, NY, United States.
Junjie GaoDepartment of Pharmacology and Toxicology, School of Medicine and Biomedical Sciences, University at Buffalo - State University of New York, Buffalo, NY, United States.
Ji-Mei ChenDepartment of Cardiovascular Surgery, Guangdong Cardiovascular Institute, Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China.
Ying GeDepartment of Cell and Regenerative Biology, School of Medicine and Public Health, University of Wisconsin - Madison, WI, United States.
Jian ZhuangDepartment of Cardiovascular Surgery, Guangdong Cardiovascular Institute, Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China. Electronic address: zhuangjianzggd@yahoo.cn.
Ji LiDepartment of Pharmacology and Toxicology, School of Medicine and Biomedical Sciences, University at Buffalo - State University of New York, Buffalo, NY, United States. Electronic address: jli23@buffalo.edu.
University at Buffalo, State University of New York · USGuangdong General Hospital · CNUniversity of Wisconsin–Madison · US

Funding

Alterations in Heart Stress Signaling during Ischemia with AgingR03AG028163 · NIA · UNIVERSITY OF WYOMING · PI LI, JI N, · 2008 to 2009
$117k
NIA NIH HHS R03 AG028163
6 · The paper itself

Abstract

aimsThe specific role of AMPKα1 or AMPKα2 in mediating cardiomyocyte contractile function remains elusive. The present study investigated how AMPK activation modulates the contractility of isolated cardiomyocytes. MAIN

methodsMechanical properties and intracellular Ca(2+) properties were measured in isolated cardiomyocytes. The stress signaling was evaluated using western blot and immunoprecipitation analysis. KEY

findingsAMPK activator, A-769662 induced maximal velocity of shortening (+dL/dt) and relengthening (-dL/dt), peak height and peak shortening (PS) amplitude in both WT and AMPKα2 KO cardiomyocytes, but did not affect time-to-90% relengthening (TR90). AMPK KD cardiomyocytes demonstrated contractile dysfunction compared with cardiomyocytes from WT and AMPKα2 KO hearts. However, the rise of intracellular Ca(2+) levels as well as intracellular ATP levels has no significant difference among WT, AMPKα2 KO and AMPK KD groups with and without the presence of A-769662. Besides, WT, AMPKα2 KO and AMPK KD group displayed a phosphorylated AMPK and downstream acetyl-CoA carboxylase (ACC) phosphorylation. Interestingly, A-769662 also triggered troponin I (cTnI) phosphorylation at Ser(149) site which is related to contractility of cardiomyocytes. Furthermore, the immunoprecipitation analysis revealed that AMPKα1 of cardiomyocytes was phosphorylated by A-769662. SIGNIFICANCE: This is the first study illustrating that activation of AMPK plays a significant role in mediating the contractile function of cardiomyocytes using transgenic animal models. AMPK activator facilitates the contractility of cardiomyocytes via activating AMPKα1 catalytic subunit. The phosphorylation of cTnI by AMPK could be a factor attributing to the regulation of contractility of cardiomyocytes.

Indexed as

AMP-Activated Protein KinasesAnimalsBiphenyl CompoundsImmunoblottingMaleMiceMice, KnockoutMice, TransgenicMyocardial ContractionMyocytes, CardiacPhosphorylationPyronesSignal TransductionThiophenesTroponin I4-hydroxy-3-(4-(2-hydroxyphenyl)phenyl)-6-oxo-7H-thieno(2,3-b)pyridine-5-carbonitrileAMP-Activated Protein KinasesBiphenyl CompoundsPyronesThiophenesTroponin IAMPKContractile functionTroponin I

Identifiers

PMID24447627
PMCPMC4777330
OpenAlexW1990560667

What OpenQuestion holds

Textmetadata
LicenceTDM
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.