Evidence map›Paper›PMID 16775082›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2006

Transverse aortic constriction leads to accelerated heart failure in mice lacking PPAR-gamma coactivator 1alpha.

Zoltan Arany, Mikhail Novikov, Sherry Chin, Yanhong Ma, Anthony Rosenzweig, Bruce M Spiegelman

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 221 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
221citing papers in PubMed, 1 pooled it
7.9field-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

221 citing papers in PubMed, 1 synthesis or guideline pooled it, 370 citations in OpenAlex.

  1. Pooled it
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  3. Article
  4. Histone Deacetylase 7 protects against pathologic cardiac hypertrophy.Journal of molecular and cellular cardiology · 2026
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  6. International journal of molecular sciences · 2025
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161 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

6 authors at 3 institutions in 1 country.

Zoltan AranyDana-Farber Cancer Institute and Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA.
Mikhail Novikov
Sherry Chin
Yanhong Ma
Anthony Rosenzweig
Bruce M Spiegelman
Harvard University · USDana-Farber Cancer Institute · USBeth Israel Deaconess Medical Center · US

Funding

PGC1 proteins, meteorin-like and energy homeostasisR01DK061562 · NIDDK · DANA-FARBER CANCER INSTITUTE · PI SPIEGELMAN, BRUCE M. · 2002 to 2018
$7.2M
PGC-1 AND NUCLEAR RECEPTORS IN ADAPTIVE THERMOGENESISR01DK054477 · NIDDK · DANA-FARBER CANCER INSTITUTE · PI SPIEGELMAN, BRUCE M. · 1998 to 2016
$7.0M
Signaling mechanisms of cardioprotection and remodelingR01HL077543 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI ROSENZWEIG, ANTHONY · 2005 to 2008
$1.6M
PGC-1 Co-Activators in Cardiac Metabolism and FunctionK08HL079172 · NHLBI · DANA-FARBER CANCER INSTITUTE · PI ARANY, ZOLTAN P · 2005 to 2009
$656k
PGC-1 and Nuclear Receptors in Adaptive ThermogenesisR56DK054477 · NIDDK · DANA-FARBER CANCER INST · PI SPIEGELMAN, BRUCE M · 2006 to 2006
$395k
NHLBI NIH HHS HL 077543NHLBI NIH HHS HL 079172NHLBI NIH HHS K08 HL079172NHLBI NIH HHS R01 HL077543NIDDK NIH HHS DK 54477NIDDK NIH HHS DK 61562NIDDK NIH HHS R01 DK054477NIDDK NIH HHS R01 DK061562NIDDK NIH HHS R56 DK054477
6 · The paper itself

Abstract

Heart failure is accompanied by important defects in metabolism. The transcriptional coactivator peroxisome proliferator-activated receptor-gamma coactivator 1alpha (PGC-1alpha) is a powerful regulator of mitochondrial biology and metabolism. PGC-1alpha and numerous genes regulated by PGC-1alpha are repressed in models of cardiac stress, such as that generated by transverse aortic constriction (TAC). This finding has suggested that PGC-1alpha repression may contribute to the maladaptive response of the heart to chronic hemodynamic loads. We show here that TAC in mice genetically engineered to lack PGC-1alpha leads to accelerated cardiac dysfunction, which is accompanied by signs of significant clinical heart failure. Treating cardiac cells in tissue culture with the catecholamine epinephrine leads to repression of PGC-1alpha and many of its target genes, recapitulating the findings in vivo in response to TAC. Importantly, introduction of ectopic PGC-1alpha can reverse the repression of most of these genes by epinephrine. Together, these data indicate that endogenous PGC-1alpha serves a cardioprotective function and suggest that repression of PGC-1alpha significantly contributes to the development of heart failure. Moreover, the data suggest that elevating PGC-1alpha activity may have therapeutic potential in the treatment of heart failure.

Indexed as

Gene Expression RegulationAnimalsAortaCardiac Output, LowConstriction, PathologicDown-RegulationEpinephrineMiceMice, KnockoutMutationMyocytes, CardiacPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaTrans-ActivatorsTranscription FactorsEpinephrinePeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPpargc1a protein, mouseTrans-ActivatorsTranscription Factors

Identifiers

PMID16775082
PMCPMC1502510
OpenAlexW2103634232

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.