Evidence map›Paper›PMID 19061437›Full record

ReviewAntioxidants & redox signaling2009

PPARs and the cardiovascular system.

Milton Hamblin, Lin Chang, Yanbo Fan, Jifeng Zhang, Y Eugene Chen

Open access · greenAbstract readReview
In one paragraph

Review in Antioxidants & redox signaling, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed
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

86 citing papers in PubMed, 210 citations in OpenAlex.

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  10. PFAS and their association with the increased risk of cardiovascular disease in postmenopausal women.Toxicological sciences : an official journal of the Society of Toxicology · 2024
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26 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

5 authors at 1 institution in 1 country.

Milton HamblinCardiovascular Center, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, Michigan 48109, USA.
Lin Chang
Yanbo Fan
Jifeng Zhang
Y Eugene Chen
University of Michigan–Ann Arbor · US

Funding

TRAINING IN MOLECULAR AND CELLULAR CARDIOLOGYT32HL007853 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI David J. Pinsky · 1996 to 2026
$11.6M
The Role of PPAR-gamma in Vascular Lesion FormationR01HL068878 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CHEN, YUQING EUGENE · 2002 to 2019
$7.6M
Nitroalkenes and Blood Pressure RegulationR01HL089544 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CHEN, YUQING EUGENE · 2008 to 2012
$2.0M
PPAR-delta in obesity-related vascular remodelingR01HL075397 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CHEN, YUQING E · 2004 to 2007
$1.7M
MicroRNA and smooth muscle cell differentiationR21HL092421 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CHEN, YUQING EUGENE · 2008 to 2009
$412k
NHLBI NIH HHS HL68878NHLBI NIH HHS HL75397NHLBI NIH HHS HL89544NHLBI NIH HHS HL92421NHLBI NIH HHS R01 HL089544NHLBI NIH HHS T32 HL007853
6 · The paper itself

Abstract

Peroxisome proliferator-activated receptors (PPARs) belong to the nuclear hormone-receptor superfamily. Originally cloned in 1990, PPARs were found to be mediators of pharmacologic agents that induce hepatocyte peroxisome proliferation. PPARs also are expressed in cells of the cardiovascular system. PPAR gamma appears to be highly expressed during atherosclerotic lesion formation, suggesting that increased PPAR gamma expression may be a vascular compensatory response. Also, ligand-activated PPAR gamma decreases the inflammatory response in cardiovascular cells, particularly in endothelial cells. PPAR alpha, similar to PPAR gamma, also has pleiotropic effects in the cardiovascular system, including antiinflammatory and antiatherosclerotic properties. PPAR alpha activation inhibits vascular smooth muscle proinflammatory responses, attenuating the development of atherosclerosis. However, PPAR delta overexpression may lead to elevated macrophage inflammation and atherosclerosis. Conversely, PPAR delta ligands are shown to attenuate the pathogenesis of atherosclerosis by improving endothelial cell proliferation and survival while decreasing endothelial cell inflammation and vascular smooth muscle cell proliferation. Furthermore, the administration of PPAR ligands in the form of TZDs and fibrates has been disappointing in terms of markedly reducing cardiovascular events in the clinical setting. Therefore, a better understanding of PPAR-dependent and -independent signaling will provide the foundation for future research on the role of PPARs in human cardiovascular biology.

Indexed as

AnimalsCardiovascular SystemEndothelial CellsHumansModels, BiologicalMuscle, Smooth, VascularPeroxisome Proliferator-Activated ReceptorsPPAR alphaPPAR deltaPPAR gammaPeroxisome Proliferator-Activated ReceptorsPPAR alphaPPAR deltaPPAR gamma

Identifiers

PMID19061437
PMCPMC2737093
OpenAlexW2076553098

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.