Evidence map›Paper›PMID 20071776›Full record

ArticleThe Journal of clinical investigation2010

Cardiomyocyte PDGFR-beta signaling is an essential component of the mouse cardiac response to load-induced stress.

Vishnu Chintalgattu, Di Ai, Robert R Langley, Jianhu Zhang, James A Bankson, Tiffany L Shih, Anilkumar K Reddy, Kevin R Coombes, Iyad N Daher, Shibani Pati and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed, 2 pooled it
10.5field-weighted citation impact, top 1% 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

91 citing papers in PubMed, 2 syntheses or guidelines pooled it, 187 citations in OpenAlex.

  1. Guideline
  2. Pooled it
  3. Recent Advances in Aptamer-Based Applications in Cardiology.International journal of molecular sciences · 2026
    Review
  4. Article
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31 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

16 authors at 4 institutions in 2 countries.

Vishnu ChintalgattuDepartment of Cardiology, University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA.
Di Ai
Robert R Langley
Jianhu Zhang
James A Bankson
Tiffany L Shih
Anilkumar K Reddy
Kevin R Coombes
Iyad N Daher
Shibani Pati
Shalin S Patel
Jennifer S Pocius
George E Taffet
L Maximillian Buja
Mark L Entman
Aarif Y Khakoo
The University of Texas MD Anderson Cancer Center · USBaylor College of Medicine · USThe University of Texas Health Science Center at Houston · USInstitute of Cardiology · PL

Funding

A Resource on Medical Ultrasonic Transducer TechnologyP41EB002182 · NIBIB · UNIVERSITY OF SOUTHERN CALIFORNIA · PI SHUNG, K KIRK · 2003 to 2016
$13.3M
ULTRASONIC INSTRUMENTATION FOR CARDIOVASCULAR STUDIESR01HL022512 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI HARTLEY, CRAIG J. · 1985 to 2012
$4.3M
Role of Blood-Borne Fibroblast Precursors in Ischemic CardiomyopathyR01HL089792 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI ENTMAN, MARK L · 2007 to 2016
$3.4M
VERY HIGH FREQUENCY (VHF) SPARSE LINEAR ARRAYSP41RR011795 · NCRR · UNIVERSITY OF SOUTHERN CALIFORNIA · PI SMITH, STEVEN · 1997 to 2002
$2.9M
Pathogenesis of Age-Related Diastolic DysfunctionR01AG017899 · NIA · BAYLOR COLLEGE OF MEDICINE · PI TAFFET, GEORGE E · 2001 to 2005
$1.9M
ANGIOTENSIN II-SMAD SIGNALING IN CARDIAC FIBROSISR01HL076661 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI ENTMAN, MARK L · 2005 to 2009
$1.6M
Howard Hughes Medical InstituteNCRR NIH HHS P41 RR011795NHLBI NIH HHS HL076661NHLBI NIH HHS HL089792NHLBI NIH HHS R01 HL022512NHLBI NIH HHS R01 HL076661NHLBI NIH HHS R01 HL089792NIA NIH HHS AG17899NIA NIH HHS R01 AG017899NIBIB NIH HHS P41 EB002182
6 · The paper itself

Abstract

PDGFR is an important target for novel anticancer therapeutics because it is overexpressed in a wide variety of malignancies. Recently, however, several anticancer drugs that inhibit PDGFR signaling have been associated with clinical heart failure. Understanding this effect of PDGFR inhibitors has been difficult because the role of PDGFR signaling in the heart remains largely unexplored. As described herein, we have found that PDGFR-beta expression and activation increase dramatically in the hearts of mice exposed to load-induced cardiac stress. In mice in which Pdgfrb was knocked out in the heart in development or in adulthood, exposure to load-induced stress resulted in cardiac dysfunction and heart failure. Mechanistically, we showed that cardiomyocyte PDGFR-beta signaling plays a vital role in stress-induced cardiac angiogenesis. Specifically, we demonstrated that cardiomyocyte PDGFR-beta was an essential upstream regulator of the stress-induced paracrine angiogenic capacity (the angiogenic potential) of cardiomyocytes. These results demonstrate that cardiomyocyte PDGFR-beta is a regulator of the compensatory cardiac response to pressure overload-induced stress. Furthermore, our findings may provide insights into the mechanism of cardiotoxicity due to anticancer PDGFR inhibitors.

Indexed as

AnimalsBody WeightCoronary CirculationHeartHeart FailureMiceMice, Inbred C57BLMice, KnockoutMyocytes, CardiacOrgan SizePhosphorylationReceptor, Platelet-Derived Growth Factor betaSignal TransductionStroke VolumeWeight-BearingReceptor, Platelet-Derived Growth Factor beta

Identifiers

PMID20071776
PMCPMC2810076
OpenAlexW2120608237

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.