ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2012
Peroxisome proliferator-activated receptor-γ protects against vascular aging.
Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.
- Relationship between PPAR-γ gene polymorphisms and ischemic stroke risk: A meta-analysis.Brain and behavior · 2021Pooled it
- PPAROxidative medicine and cellular longevity · 2021Article
- PPARγ and RhoBTB1 in hypertension.Current opinion in nephrology and hypertension · 2020Review
- Effects and Mechanisms of Five Psoralea Prenylflavonoids on Aging-Related Diseases.Oxidative medicine and cellular longevity · 2020Review
- Endothelial PPARγ Is Crucial for Averting Age-Related Vascular Dysfunction by Stalling Oxidative Stress and ROCK.Neurotoxicity research · 2019Review
- Restoring mitochondrial DNA copy number preserves mitochondrial function and delays vascular aging in mice.Aging cell · 2018Article
- Endothelial PPARγ (Peroxisome Proliferator-Activated Receptor-γ) Is Essential for Preventing Endothelial Dysfunction With Aging.Hypertension (Dallas, Tex. : 1979) · 2018Article
- High Serum Levels of Malondialdehyde and 8-OHdG are both Associated with Early Cognitive Impairment in Patients with Acute Ischaemic Stroke.Scientific reports · 2017Article
- Cerebral Small Vessel Disease: Targeting Oxidative Stress as a Novel Therapeutic Strategy?Frontiers in pharmacology · 2016Review
- Prostanoid-mediated contractions of the carotid artery become Nox2-independent with aging.Age (Dordrecht, Netherlands) · 2015Article
- The Role of Oxidative Damage in the Pathogenesis and Progression of Alzheimer's Disease and Vascular Dementia.Oxidative medicine and cellular longevity · 2015Review
- Functional heterogeneity of NADPH oxidase-mediated contractions to endothelin with vascular aging.Life sciences · 2014Article
- Endothelin-1 but not angiotensin II contributes to functional aging in murine carotid arteries.Life sciences · 2014Article
- Sex and basic science. A Title IX position.American journal of physiology. Regulatory, integrative and comparative physiology · 2014Article
- Interleukin-10 protects against aging-induced endothelial dysfunction.Physiological reports · 2013Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Vascular disease occurs commonly during aging. Carotid artery and cerebrovascular disease are major causes of stroke and contributors to dementia. Recent evidence suggests that peroxisome proliferator-activated receptor-γ (PPARγ) may play a protective role in the vasculature, but the potential importance of PPARγ in vascular aging is unknown. To examine the hypothesis that PPARγ normally protects against vascular aging, we studied heterozygous knockin mice expressing a human dominant-negative mutation in PPARγ (P465L, designated L/+). Endothelial dysfunction, a major contributor to vascular disease, was studied using carotid arteries from adult (8 ± 1 mo) and old (24 ± 1 mo) L/+ mice and wild-type littermates. In arteries from wild-type mice, responses to the endothelium-dependent agonist ACh were similar in adult and old wild-type mice but were reduced by ∼50% in old L/+ mice (n = 7-10, P < 0.05). Impaired responses in arteries from old L/+ mice were restored to normal by a scavenger of superoxide. Relaxation of arteries to nitroprusside (an NO donor) was similar in all groups. Contraction of arteries to U46619 was not affected by age or genotype, while maximal responses to endothelin-1 were reduced with age in both wild-type and L/+ mice. Vascular expression (mRNA) of the catalytic component of NADPH oxidase (Nox2) was not altered in wild-type mice but was increased significantly in old L/+ mice. These findings provide the first evidence that interference with PPARγ function accelerates vascular aging, suggesting a novel role for PPARγ in protecting against age-induced oxidative stress and endothelial dysfunction.
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Registered trials
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.