Evidence map›Paper›PMID 22135402›Full record

ArticleCirculation. Heart failure2012

Akt1-mediated skeletal muscle growth attenuates cardiac dysfunction and remodeling after experimental myocardial infarction.

Satoshi Araki, Yasuhiro Izumiya, Shinsuke Hanatani, Taku Rokutanda, Hiroki Usuku, Yuichi Akasaki, Toru Takeo, Naomi Nakagata, Kenneth Walsh, Hisao Ogawa

Abstract read
In one paragraph

Article in Circulation. Heart failure, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

22 citing papers in PubMed, 51 citations in OpenAlex.

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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

10 authors at 1 institution in 1 country.

Satoshi ArakiDepartment of Cardiovascular Medicine, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.
Yasuhiro Izumiya
Shinsuke Hanatani
Taku Rokutanda
Hiroki Usuku
Yuichi Akasaki
Toru Takeo
Naomi Nakagata
Kenneth Walsh
Hisao Ogawa
Boston University · US

Funding

Redox regulation in Endothelial Progenitor CellsP01HL081587 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI WALSH, KENNETH · 2005 to 2015
$21.5M
REGULATION OF VESSEL WALL APOPTOSISR37AG015052 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI WALSH, KENNETH · 2003 to 2012
$4.0M
SIGNALING PATHWAYS IN HEART FAILURER01HL077774 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI WALSH, KENNETH · 2005 to 2009
$1.9M
Muscle loss and metabolic dysfunction associated with agingR01AG034972 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI WALSH, KENNETH · 2010 to 2014
$1.6M
REGULATION OF VESSEL WALL APOPTOSISR01AG015052 · NIA · CARITAS ST. ELIZABETH'S MEDICAL CENTER · PI WALSH, KENNETH · 1998 to 2002
$1.0M
NHLBI NIH HHS P01 HL081587NHLBI NIH HHS R01 HL077774NIA NIH HHS AG34972NIA NIH HHS R01 AG015052NIA NIH HHS R01 AG034972NIA NIH HHS R37 AG015052
6 · The paper itself

Abstract

backgroundIt is appreciated that aerobic endurance exercise can attenuate unfavorable myocardial remodeling following myocardial infarction. In contrast, little is known about the effects of increasing skeletal muscle mass, typically achieved through resistance training, on this process. Here, we utilized transgenic (TG) mice that can induce the growth of functional skeletal muscle by switching Akt1 signaling in muscle fibers to assess the impact of glycolytic muscle growth on post-myocardial infarction cardiac remodeling. METHODS AND

resultsMale-noninduced TG mice and their nontransgenic littermates (control) were subjected to left anterior coronary artery ligation. Two days after surgery, mice were provided doxycycline in their drinking water to activate Akt1 transgene expression in a skeletal muscle-specific manner. Myogenic Akt1 activation led to diminished left ventricular dilation and reduced contractile dysfunction compared with control mice. Improved cardiac function in Akt1 TG mice was coupled to diminished myocyte hypertrophy, decreased interstitial fibrosis, and increased capillary density. ELISA and protein array analyses demonstrated that serum levels of proangiogenic growth factors were upregulated in Akt1 TG mice compared with control mice. Cardiac eNOS was activated in Akt1 TG mice after myocardial infarction. The protective effect of skeletal muscle Akt activation on cardiac remodeling and systolic function was abolished by treatment with the eNOS inhibitor l-NAME.

conclusionsAkt1-mediated skeletal muscle growth attenuates cardiac remodeling after myocardial infarction and is associated with an increased capillary density in the heart. This improvement appears to be mediated by skeletal muscle to cardiac communication, leading to activation of eNOS-signaling in the heart.

Indexed as

Ventricular RemodelingAnimalsEnzyme InhibitorsFibroblast Growth Factor 1Heart VentriclesMaleMiceMice, Inbred C57BLMice, TransgenicModels, AnimalMuscle, SkeletalMyocardial InfarctionNG-Nitroarginine Methyl EsterNitric Oxide Synthase Type IIIProto-Oncogene Proteins c-aktSignal TransductionAkt1 protein, mouseEnzyme InhibitorsFibroblast Growth Factor 1NG-Nitroarginine Methyl EsterNitric Oxide Synthase Type IIIProto-Oncogene Proteins c-aktVascular Endothelial Growth Factor A

Identifiers

PMID22135402
PMCPMC3670415
OpenAlexW2165136585

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.