Evidence map›Paper›PMID 19001090›Full record

ArticleMolecular and cellular biology2009

Deletion of Shp2 tyrosine phosphatase in muscle leads to dilated cardiomyopathy, insulin resistance, and premature death.

Frederic Princen, Emilie Bard, Farah Sheikh, Sharon S Zhang, Jing Wang, Wagner M Zago, Dongmei Wu, Ramon Diaz Trelles, Beatrice Bailly-Maitre, C Ronald Kahn and 6 more

Abstract read
In one paragraph

Article in Molecular and cellular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

40 citing papers in PubMed, 69 citations in OpenAlex.

  1. The βCirculation research · 2025
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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

16 authors at 5 institutions in 2 countries.

Frederic PrincenBurnham Institute for Medical Research, 10901 N. Torrey Pines Rd., La Jolla, CA 92037, USA.
Emilie Bard
Farah Sheikh
Sharon S Zhang
Jing Wang
Wagner M Zago
Dongmei Wu
Ramon Diaz Trelles
Beatrice Bailly-Maitre
C Ronald Kahn
Yan Chen
John C Reed
Gary G Tong
Mark Mercola
Ju Chen
Gen-Sheng Feng
Sanford Burnham Prebys Medical Discovery Institute · USUniversity of California, San Diego · USChinese Academy of Sciences · CNHarvard University · USXiamen University · CN

Funding

Regulation of Leptin SignalingR01DK073945 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI FENG, GEN-SHENG · 2007 to 2010
$1.5M
(FHL1) in Signaling Pathways of Cardiac Hypertrophy and DiseaseR01HL082902 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI CHEN, JU · 2006 to 2009
$1.5M
MOLECULAR BIOLOGY OF HEART INDUCTIONR01HL059502 · NHLBI · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI MERCOLA, MARK · 1997 to 2005
$1.4M
NHLBI NIH HHS R01 HL059502NHLBI NIH HHS R01HL059502NHLBI NIH HHS R01 HL082902NHLBI NIH HHS R01HL082902NIDDK NIH HHS R01 DK073945NIDDK NIH HHS R01DK73945
6 · The paper itself

Abstract

The intracellular signaling mechanisms underlying the pathogenesis of cardiac diseases are not fully understood. We report here that selective deletion of Shp2, an SH2-containing cytoplasmic tyrosine phosphatase, in striated muscle results in severe dilated cardiomyopathy in mice, leading to heart failure and premature mortality. Development of cardiomyopathy in this mouse model is coupled with insulin resistance, glucose intolerance, and impaired glucose uptake in striated muscle cells. Shp2 deficiency leads to upregulation of leukemia inhibitory factor-stimulated phosphatidylinositol 3-kinase/Akt, Erk5, and Stat3 pathways in cardiomyocytes. Insulin resistance and impaired glucose uptake in Shp2-deficient mice are at least in part due to impaired protein kinase C-zeta/lambda and AMP-kinase activities in striated muscle. Thus, we have generated a mouse line modeling human patients suffering from cardiomyopathy and insulin resistance. This study reinforces a concept that a compound disease with multiple cardiovascular and metabolic disturbances can be caused by a defect in a single molecule such as Shp2, which modulates multiple signaling pathways initiated by cytokines and hormones.

Indexed as

Insulin ResistanceAnimalsCardiomyopathy, DilatedGene DeletionGlucoseGlucose IntoleranceHeartKaplan-Meier EstimateLeukemia Inhibitory FactorMAP Kinase Kinase KinasesMiceMice, KnockoutMitogen-Activated Protein Kinase 7Muscle, SkeletalMyocardiumPhosphatidylinositol 3-KinasesAkt1 protein, mouseGlucoseinsulin-stimulated MEK kinaseLeukemia Inhibitory FactorLif protein, mouseMAP Kinase Kinase KinasesMitogen-Activated Protein Kinase 7Phosphatidylinositol 3-KinasesProtein Tyrosine Phosphatase, Non-Receptor Type 11Proto-Oncogene Proteins c-aktPtpn11 protein, mouseStat3 protein, mouseSTAT3 Transcription Factor

Identifiers

PMID19001090
PMCPMC2612510
OpenAlexW2096646959

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.