Evidence map›Paper›PMID 21724622›Full record

ReviewEuropean journal of heart failure2011

AKT signalling in the failing heart.

Antoine H Chaanine, Roger J Hajjar

Open access · bronzeAbstract readReview
In one paragraph

Review in European journal of heart failure, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
106citing papers in PubMed, 2 pooled it
8.2field-weighted citation impact, top 2% 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

106 citing papers in PubMed, 2 syntheses or guidelines pooled it, 183 citations in OpenAlex.

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  19. Endothelial cell-specific mineralocorticoid receptor activation promotes diastolic dysfunction in diet-induced obese male mice.American journal of physiology. Regulatory, integrative and comparative physiology · 2023
    Article
  20. Dietary NWorld journal of diabetes · 2022
    Article

46 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Antoine H ChaanineCardiovascular Research Center, Mount Sinai School of Medicine, New York, NY, USA.
Roger J Hajjar
Mount Sinai Hospital · US

Funding

TRAINING PROGRAM IN MOLECULAR AND CELLULAR CARDIOLOGYT32HL007824 · NHLBI · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI GELB, BRUCE D · 1995 to 2022
$8.6M
PICOT and Cardiac HypertrophyR01HL080498 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI HAJJAR, ROGER J. · 2006 to 2010
$2.2M
Targeting Calcium Cycling in Pre-Clinical Model CardiacR01HL083156 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI HAJJAR, ROGER J. · 2006 to 2010
$1.7M
C-TRIP: Targeted Gene Therapy for the Treatment of Heart Failure (P20)P20HL100396 · NHLBI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI HAJJAR, ROGER J. · 2010 to 2011
$1.7M
Gene Therapy with Cardiotropic Vectors for the Treatment of Heart FailureR01HL088434 · NHLBI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI HAJJAR, ROGER J. · 2010 to 2013
$1.7M
K and Ca Channels in Cardiac Hypertrophy and FailureR01HL071763 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI HAJJAR, ROGER J. · 2003 to 2006
$1.6M
Regression of cardiac hypertrophyR01HL093183 · NHLBI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI HAJJAR, ROGER J. · 2009 to 2010
$1.1M
NHLBI NIH HHS HL071763NHLBI NIH HHS HL080498NHLBI NIH HHS HL083156NHLBI NIH HHS HL088434NHLBI NIH HHS P20HL100396NHLBI NIH HHS R01 HL093183NHLBI NIH HHS T32 HL007824
6 · The paper itself

Abstract

AKT is a serine/threonine protein kinase, also known as protein kinase B, which regulates cardiac growth, myocardial angiogenesis, glucose metabolism, and cell death in cardiac myocytes. AKT is activated by its phosphorylation at Thr 308 and ser 473 by PDK1 and mTORC2, respectively, in response to trophic stimuli such as insulin and insulin growth factor. c-Jun N-Terminal Kinases (JNKs) phosphorylate AKT at Thr 450 and potentiate its interaction with its downstream effectors. The short-term activation of AKT promotes physiological hypertrophy and protection from myocardial injury; whereas, its long-term activation causes pathological hypertrophy and heart failure. In this review we will discuss the role of AKT in regulating signalling pathways in the heart with special emphasis on the role of AKT in modulating stress induced autophagic cell death in cardiomyocytes in vitro.

Indexed as

AnimalsApoptosisAutophagyCoronary VesselsDisease Models, AnimalHeart FailureHumansMiceMyocytes, CardiacNeovascularization, PathologicProto-Oncogene Proteins c-aktSignal TransductionProto-Oncogene Proteins c-akt

Identifiers

PMID21724622
PMCPMC3143831
OpenAlexW2104705785

What Socratic 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 Socratic graph.