Evidence map›Paper›PMID 27312223›Full record

ReviewArteriosclerosis, thrombosis, and vascular biology2016

Role of PGC-1α in Vascular Regulation: Implications for Atherosclerosis.

Andrew O Kadlec, Dawid S Chabowski, Karima Ait-Aissa, David D Gutterman

Open access · bronzeAbstract readReview
In one paragraph

Review in Arteriosclerosis, thrombosis, and vascular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed, 1 pooled it
3.9field-weighted citation impact, top 6% 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

57 citing papers in PubMed, 1 synthesis or guideline pooled it, 93 citations in OpenAlex.

  1. Pooled it
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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

4 authors at 1 institution in 1 country.

Andrew O KadlecFrom the Department of Physiology (A.O.K., D.D.G.), Division of Cardiology, Department of Medicine (D.S.C., K.A.-A., D.D.G.), and Cardiovascular Center (A.O.K., D.S.C., K.A.-A., D.D.G.), Medical College of Wisconsin, Milwaukee; and Department of Veterans Administration Medical Center, Milwaukee, WI (D.D.G.).
Dawid S ChabowskiFrom the Department of Physiology (A.O.K., D.D.G.), Division of Cardiology, Department of Medicine (D.S.C., K.A.-A., D.D.G.), and Cardiovascular Center (A.O.K., D.S.C., K.A.-A., D.D.G.), Medical College of Wisconsin, Milwaukee; and Department of Veterans Administration Medical Center, Milwaukee, WI (D.D.G.).
Karima Ait-AissaFrom the Department of Physiology (A.O.K., D.D.G.), Division of Cardiology, Department of Medicine (D.S.C., K.A.-A., D.D.G.), and Cardiovascular Center (A.O.K., D.S.C., K.A.-A., D.D.G.), Medical College of Wisconsin, Milwaukee; and Department of Veterans Administration Medical Center, Milwaukee, WI (D.D.G.).
David D GuttermanFrom the Department of Physiology (A.O.K., D.D.G.), Division of Cardiology, Department of Medicine (D.S.C., K.A.-A., D.D.G.), and Cardiovascular Center (A.O.K., D.S.C., K.A.-A., D.D.G.), Medical College of Wisconsin, Milwaukee; and Department of Veterans Administration Medical Center, Milwaukee, WI (D.D.G.). dgutt@mcw.edu.
United States Department of Veterans Affairs · US

Funding

Medical Scientist Training ProgramT32GM080202 · NIGMS · MEDICAL COLLEGE OF WISCONSIN · PI BARBIERI, JOSEPH T, SALZMAN, NITA H · 2010 to 2024
$5.7M
Mechanism of Flow-Induced Dilation in the Human MicrocirculationR01HL113612 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI GUTTERMAN, DAVID D. · 2013 to 2016
$1.7M
NHLBI NIH HHS R01 HL113612NIGMS NIH HHS T32 GM080202
6 · The paper itself

Abstract

Mitochondrial dysfunction results in high levels of oxidative stress and mitochondrial damage, leading to disruption of endothelial homeostasis. Recent discoveries have clarified several pathways, whereby mitochondrial dysregulation contributes to endothelial dysfunction and vascular disease burden. One such pathway centers around peroxisome proliferator receptor-γ coactivator 1α (PGC-1α), a transcriptional coactivator linked to mitochondrial biogenesis and antioxidant defense, among other functions. Although primarily investigated for its therapeutic potential in obesity and skeletal muscle differentiation, the ability of PGC-1α to alter a multitude of cellular functions has sparked interest in its role in the vasculature. Within this context, recent studies demonstrate that PGC-1α plays a key role in endothelial cell and smooth muscle cell regulation through effects on oxidative stress, apoptosis, inflammation, and cell proliferation. The ability of PGC-1α to affect these parameters is relevant to vascular disease progression, particularly in relation to atherosclerosis. Upregulation of PGC-1α can prevent the development of, and even encourage regression of, atherosclerotic lesions. Therefore, PGC-1α is poised to serve as a promising target in vascular disease. This review details recent findings related to PGC-1α in vascular regulation, regulation of PGC-1α itself, the role of PGC-1α in atherosclerosis, and therapies that target this key protein.

Indexed as

AnimalsApoptosisAtherosclerosisCell ProliferationEndothelial CellsEndothelium, VascularGene Expression RegulationHumansInflammationMitochondria, MuscleMuscle, Smooth, VascularMyocytes, Smooth MuscleOxidative StressPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPlaque, AtheroscleroticSignal TransductionPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPPARGC1A protein, humanapoptosisatherosclerosiscardiovascular diseaseendotheliumoxidative stress

Identifiers

PMID27312223
PMCPMC4965312
OpenAlexW2570800839

What OpenQuestion holds

Textmetadata
LicenceTDM
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.