Evidence map›Paper›PMID 27910955›Full record

ArticleScientific reports2016

PGC-1α dictates endothelial function through regulation of eNOS expression.

Siobhan M Craige, Swenja Kröller-Schön, Chunying Li, Shashi Kant, Shenghe Cai, Kai Chen, Mayur M Contractor, Yongmei Pei, Eberhard Schulz, John F Keaney

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

38 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
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  7. Endothelial TERT drives microvascular phenotype associated with coronary artery disease.American journal of physiology. Heart and circulatory physiology · 2025
    Article
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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 2 institutions in 2 countries.

Siobhan M CraigeDivision of Cardiovascular Medicine, Department of Medicine, University of Massachusetts Medical School, Worcester, MA, USA.
Swenja Kröller-SchönDepartment of Cardiology Medizinische Klinik und Poliklinik Universitätsmedizin Mainz, Mainz, Germany.
Chunying LiDivision of Cardiovascular Medicine, Department of Medicine, University of Massachusetts Medical School, Worcester, MA, USA.
Shashi KantDivision of Cardiovascular Medicine, Department of Medicine, University of Massachusetts Medical School, Worcester, MA, USA.
Shenghe CaiDivision of Cardiovascular Medicine, Department of Medicine, University of Massachusetts Medical School, Worcester, MA, USA.
Kai ChenDepartment of Cardiology Medizinische Klinik und Poliklinik Universitätsmedizin Mainz, Mainz, Germany.
Mayur M ContractorDivision of Cardiovascular Medicine, Department of Medicine, University of Massachusetts Medical School, Worcester, MA, USA.
Yongmei PeiDivision of Cardiovascular Medicine, Department of Medicine, University of Massachusetts Medical School, Worcester, MA, USA.
Eberhard SchulzDepartment of Cardiology Medizinische Klinik und Poliklinik Universitätsmedizin Mainz, Mainz, Germany.
John F KeaneyDivision of Cardiovascular Medicine, Department of Medicine, University of Massachusetts Medical School, Worcester, MA, USA.
University of Massachusetts Chan Medical School · USKlinik und Poliklinik für Psychosomatische Medizin und Psychotherapie · DE

Funding

Nox4 and Vascular HomeostasisR01HL098407 · NHLBI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI KEANEY, JOHN FRANCIS · 2010 to 2017
$3.8M
Mitochondrial Modulation of Endothelia FunctionR01HL092122 · NHLBI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI KEANEY, JOHN FRANCIS · 2009 to 2016
$3.3M
Nox 4 modulation of NO bioavailability and vascular functionF32HL099282 · NHLBI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI CRAIGE, SIOBHAN M · 2010 to 2012
$159k
NHLBI NIH HHS F32 HL099282NHLBI NIH HHS R01 HL092122NHLBI NIH HHS R01 HL098407
6 · The paper itself

Abstract

Endothelial dysfunction is a characteristic of many vascular related diseases such as hypertension. Peroxisome proliferator activated receptor gamma, coactivator 1α (PGC-1α) is a unique stress sensor that largely acts to promote adaptive responses. Therefore, we sought to define the role of endothelial PGC-1α in vascular function using mice with endothelial specific loss of function (PGC-1α EC KO) and endothelial specific gain of function (PGC-1α EC TG). Here we report that endothelial PGC-1α is suppressed in angiotensin-II (ATII)-induced hypertension. Deletion of endothelial PGC-1α sensitized mice to endothelial dysfunction and hypertension in response to ATII, whereas PGC-1α EC TG mice were protected. Mechanistically, PGC-1α promotes eNOS expression and activity, which is necessary for protection from ATII-induced dysfunction as mice either treated with an eNOS inhibitor (LNAME) or lacking eNOS were no longer responsive to transgenic endothelial PGC-1α expression. Finally, we determined that the orphan nuclear receptor, estrogen related receptor α (ERRα) is required to coordinate the PGC-1α -induced eNOS expression. In conclusion, endothelial PGC-1α expression protects from vascular dysfunction by promoting NO• bioactivity through ERRα induced expression of eNOS.

Indexed as

Gene Expression Regulation, EnzymologicAngiotensin IIAnimalsCell LineEndothelial CellsEstrogen Receptor alphaHumansHypertensionMiceMice, KnockoutNitric OxideNitric Oxide Synthase Type IIIPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaAngiotensin IIEstrogen Receptor alphaNitric OxideNitric Oxide Synthase Type IIINos3 protein, mousePeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPpargc1a protein, mouse

Identifiers

PMID27910955
PMCPMC5133545
OpenAlexW2559210931

What OpenQuestion holds

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Registered trials

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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.