Evidence map›Paper›PMID 19477967›Full record

ArticleCardiovascular research2009

AMP-activated protein kinase confers protection against TNF-{alpha}-induced cardiac cell death.

Girish Kewalramani, Prasanth Puthanveetil, Fang Wang, Min Suk Kim, Sylvia Deppe, Ashraf Abrahani, Dan S Luciani, James D Johnson, Brian Rodrigues

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Cardiovascular research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
6.1field-weighted citation impact, top 3% 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

36 citing papers in PubMed, 66 citations in OpenAlex.

  1. Article
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  4. Review
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  8. Metformin Protects against HMolecular therapy. Nucleic acids · 2018
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  10. A Linear Fragment of Unacylated Ghrelin (UAGFrontiers in endocrinology · 2018
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Glucocorticoid signaling in the heart: A cardiomyocyte perspective.The Journal of steroid biochemistry and molecular biology · 2015
    Review
  16. Article
  17. Article
  18. Article
  19. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 1 institution in 1 country.

Girish KewalramaniDivision of Pharmacology and Toxicology, Faculty of Pharmaceutical Sciences, The University of British Columbia, Vancouver, BC, Canada.
Prasanth Puthanveetil
Fang Wang
Min Suk Kim
Sylvia Deppe
Ashraf Abrahani
Dan S Luciani
James D Johnson
Brian Rodrigues
University of British Columbia · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsAlthough a substantial role for 5' adenosine monophosphate-activated protein kinase (AMPK) has been established in regulating cardiac metabolism, a less studied action of AMPK is its ability to prevent cardiac cell death. Using established AMPK activators like dexamethasone (DEX) or metformin (MET), the objective of the present study was to determine whether AMPK activation prevents tumour necrosis factor-alpha (TNF-alpha) induced apoptosis in adult rat ventricular cardiomyocytes. METHODS AND

resultsCardiomyocytes were incubated with DEX, MET, or TNF-alpha for varying durations (0-12 h). TNF-alpha-induced cell damage was evaluated by measuring caspase-3 activity and Hoechst staining. Protein and gene estimation techniques were employed to determine the mechanisms mediating the effects of AMPK activators on TNF-alpha-induced cardiomyocyte apoptosis. Incubation of myocytes with TNF-alpha for 8 h has increased caspase-3 activation and apoptotic cell death, an effect that was abrogated by DEX and MET. The beneficial effect of DEX and MET was associated with stimulation of AMPK, which led to a rapid and sustained increase in Bad phosphorylation. This event reduced the interaction between Bad and Bcl-xL, limiting cytochrome c release and caspase-3 activation. Addition of Compound C to inhibit AMPK reduced Bad phosphorylation and prevented the beneficial effects of AMPK against TNF-alpha-induced cytotoxicity.

conclusionOur data demonstrate that although DEX and MET are used as anti-inflammatory agents or insulin sensitizers, respectively, their common property to phosphorylate AMPK promotes cardiomyocyte cell survival through its regulation of Bad and the mitochondrial apoptotic mechanism.

Indexed as

ApoptosisAMP-Activated Protein KinasesAnimalsbcl-Associated Death ProteinCalciumCalcium-Calmodulin-Dependent Protein Kinase Type 1Caspase 3Cytochromes cDexamethasoneMaleMyocytes, CardiacPhosphorylationProto-Oncogene Proteins c-metRatsRats, WistarTumor Necrosis Factor-alphaAMP-Activated Protein KinasesBad protein, ratbcl-Associated Death ProteinCalciumCalcium-Calmodulin-Dependent Protein Kinase Type 1Camk1 protein, ratCaspase 3Cytochromes cDexamethasoneProto-Oncogene Proteins c-metTumor Necrosis Factor-alpha

Identifiers

PMID19477967
OpenAlexW2088683504

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.