ArticleHypertension (Dallas, Tex. : 1979)2014
Role of peroxisome proliferator-activated receptor-γ in vascular muscle in the cerebral circulation.
Article in Hypertension (Dallas, Tex. : 1979), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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
21 citing papers in PubMed, 27 citations in OpenAlex.
- Role of the Renin-Angiotensin System in Blood Pressure Regulation in Smooth Muscle-Specific Cullin-3 Deficient Mice.Hypertension (Dallas, Tex. : 1979) · 2025Article
- Hypertension: Causes and Consequences of Circadian Rhythms in Blood Pressure.Circulation research · 2024Review
- The 2023 Walter B. Cannon Award Lecture: Mechanisms Regulating Vascular Function and Blood Pressure by the PPARγ-RhoBTB1-CUL3 Pathway.Function (Oxford, England) · 2024Review
- Activation of the Central Renin-Angiotensin System Causes Local Cerebrovascular Dysfunction.Stroke · 2021Article
- Role of the Peroxisome Proliferator Activated Receptors in Hypertension.Circulation research · 2021Review
- Contributions of Aging to Cerebral Small Vessel Disease.Annual review of physiology · 2020Review
- Conditional deletion of smooth muscle Cullin-3 causes severe progressive hypertension.JCI insight · 2019Article
- Interference With Endothelial PPAR (Peroxisome Proliferator-Activated Receptor)-γ Causes Accelerated Cerebral Vascular Dysfunction in Response to Endogenous Renin-Angiotensin System Activation.Hypertension (Dallas, Tex. : 1979) · 2018Article
- Endothelial PPARγ (Peroxisome Proliferator-Activated Receptor-γ) Is Essential for Preventing Endothelial Dysfunction With Aging.Hypertension (Dallas, Tex. : 1979) · 2018Article
- Genetic Interference With Endothelial PPAR-γ (Peroxisome Proliferator-Activated Receptor-γ) Augments Effects of Angiotensin II While Impairing Responses to Angiotensin 1-7.Hypertension (Dallas, Tex. : 1979) · 2017Article
- Retinol-binding protein 7 is an endothelium-specific PPARJCI insight · 2017Article
- Cerebral Vascular Disease and Neurovascular Injury in Ischemic Stroke.Circulation research · 2017Review
- Cullin-3 mutation causes arterial stiffness and hypertension through a vascular smooth muscle mechanism.JCI insight · 2016Article
- Heterogeneous Impact of ROCK2 on Carotid and Cerebrovascular Function.Hypertension (Dallas, Tex. : 1979) · 2016Article
- Microvascular Dysfunction and Cognitive Impairment.Cellular and molecular neurobiology · 2016Review
- Interference with PPARγ in endothelium accelerates angiotensin II-induced endothelial dysfunction.Physiological genomics · 2016Article
- PPARγ Regulation in Hypertension and Metabolic Syndrome.Current hypertension reports · 2015Review
- Impacts of Alternative Splicing Events on the Differentiation of Adipocytes.International journal of molecular sciences · 2015Review
- Smooth Muscle Peroxisome Proliferator-Activated Receptor γ Plays a Critical Role in Formation and Rupture of Cerebral Aneurysms in Mice In Vivo.Hypertension (Dallas, Tex. : 1979) · 2015Article
- Molecular mechanisms regulating vascular tone by peroxisome proliferator activated receptor gamma.Current opinion in nephrology and hypertension · 2015Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Although peroxisome proliferator-activated receptor-γ (PPARγ) is thought to play a protective role in the vasculature, its cell-specific effect, particularly in resistance vessels, is poorly defined. Nitric oxide (NO) plays a major role in vascular biology in the brain. We examined the hypothesis that selective interference with PPARγ in vascular muscle would impair NO-dependent responses and augment vasoconstrictor responses in the cerebral circulation. We studied mice expressing a dominant negative mutation in human PPARγ (P467L) under the control of the smooth muscle myosin heavy chain promoter (S-P467L). In S-P467L mice, dilator responses to exogenously applied or endogenously produced NO were greatly impaired in cerebral arteries in vitro and in small cerebral arterioles in vivo. Select NO-independent responses, including vasodilation to low concentrations of potassium, were also impaired in S-P467L mice. In contrast, increased expression of wild-type PPARγ in smooth muscle had little effect on vasomotor responses. Mechanisms underlying impairment of both NO-dependent and NO-independent vasodilator responses after interference with PPARγ involved Rho kinase with no apparent contribution by oxidative stress-related mechanisms. These findings support the concept that via effects on Rho kinase-dependent signaling, PPARγ in vascular muscle is a major determinant of vascular tone in resistance vessels and, in particular, NO-mediated signaling in cerebral arteries and brain microvessels. Considering the importance of NO and Rho kinase, these findings have implications for regulation of cerebral blood flow and the pathogenesis of large and small vessel disease in brain.
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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.