ArticleHypertension (Dallas, Tex. : 1979)2012
Peroxisome proliferator-activated receptor-γ regulates inflammation and renin-angiotensin system activity in the hypothalamic paraventricular nucleus and ameliorates peripheral manifestations of heart failure.
Article in Hypertension (Dallas, Tex. : 1979), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 38 citations in OpenAlex.
- RORγt Mediates Angiotensin II-Induced Pressor Responses, Microglia Activation, and Neuroinflammation by Disrupting the Blood-Brain Barrier in Rats.Journal of the American Heart Association · 2025Article
- Abscisic acid regulates maternal behavior in rats via PPARγ receptors and hypothalamic oxytocin signaling.Iranian journal of veterinary research · 2025Article
- Article
- A high-throughput drug screening identifies luteolin as a therapeutic candidate for pathological cardiac hypertrophy and heart failure.Frontiers in cardiovascular medicine · 2023Article
- Angiotensin II inhibits the A-type KAmerican journal of physiology. Regulatory, integrative and comparative physiology · 2022Article
- Article
- Reducing brain TACE activity improves neuroinflammation and cardiac function in heart failure rats.Frontiers in physiology · 2022Article
- Regulatory mechanism of fibrosis-related genes in patients with heart failure.Frontiers in genetics · 2022Article
- Article
- Role of the Peroxisome Proliferator Activated Receptors in Hypertension.Circulation research · 2021Review
- Sex differences in the central and peripheral manifestations of ischemia-induced heart failure in rats.American journal of physiology. Heart and circulatory physiology · 2019Article
- Inhibition of inflammation by minocycline improves heart failure and depression-like behaviour in rats after myocardial infarction.PloS one · 2019Article
- Differentially expressed genes in PPARγ-deficient MSCs.Molecular and cellular endocrinology · 2018Article
- Angiotensin II Type 1a Receptors in the Subfornical Organ Modulate Neuroinflammation in the Hypothalamic Paraventricular Nucleus in Heart Failure Rats.Neuroscience · 2018Article
- Interplay between the renin-angiotensin system, the canonical WNT/β-catenin pathway and PPARγ in hypertension.Current hypertension reports · 2018Review
- Blood-borne interleukin-1β acts on the subfornical organ to upregulate the sympathoexcitatory milieu of the hypothalamic paraventricular nucleus.American journal of physiology. Regulatory, integrative and comparative physiology · 2018Article
- TNF-α receptor 1 knockdown in the subfornical organ ameliorates sympathetic excitation and cardiac hemodynamics in heart failure rats.American journal of physiology. Heart and circulatory physiology · 2017Article
- Pomegranate extract decreases oxidative stress and alleviates mitochondrial impairment by activating AMPK-Nrf2 in hypothalamic paraventricular nucleus of spontaneously hypertensive rats.Scientific reports · 2016Article
- ERK1/2 MAPK signaling in hypothalamic paraventricular nucleus contributes to sympathetic excitation in rats with heart failure after myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2016Article
- Neurotransmission to parasympathetic cardiac vagal neurons in the brain stem is altered with left ventricular hypertrophy-induced heart failure.American journal of physiology. Heart and circulatory physiology · 2015Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Activation of peroxisome proliferator-activated receptor (PPAR)-γ, a nuclear transcription factor, has been shown to inhibit the production of proinflammatory cytokines and, in peripheral tissues, to downregulate the renin-angiotensin system. PPAR-γ is expressed in key brain areas involved in cardiovascular and autonomic regulation. We hypothesized that activation of central PPAR-γ would reduce sympathetic excitation and ameliorate peripheral manifestations of heart failure (HF) by inhibiting central inflammation and brain renin-angiotensin system activity. Two weeks after coronary artery ligation, HF rats received an intracerebroventricular infusion of the PPAR-γ agonist pioglitazone or vehicle for another 2 weeks. PPAR-γ expression in the paraventricular nucleus of hypothalamus, an important cardiovascular region, was unchanged in HF compared with sham-operated rats. However, PPAR-γ DNA binding activity was reduced, nuclear factor-κB activity was increased, and expression of proinflammatory cytokines and angiotensin II type-1 receptor was augmented in the HF rats. Mean blood pressure response to ganglionic blockade was greater; plasma norepinephrine levels, lung/body weight, right ventricle/body weight, and left ventricular end-diastolic pressure were increased; and maximal left ventricular dP/dt was decreased. All of these findings were ameliorated in HF rats treated with intracerebroventricular pioglitazone, which increased PPAR-γ expression and DNA binding activity in the paraventricular nucleus of hypothalamus. The results demonstrate that cardiovascular and autonomic mechanisms leading to heart failure after myocardial infarction can be modulated by activation of PPAR-γ in the brain. Central PPAR-γ may be a novel target for treatment of sympathetic excitation in myocardial infarction-induced HF.
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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.