ArticlePPAR research2013
Effects of PPAR γ Agonist Pioglitazone on Redox-Sensitive Cellular Signaling in Young Spontaneously Hypertensive Rats.
Article in PPAR research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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.
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.
Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- Pioglitazone mitigates early brain injury by suppressing neuroinflammation and oxidative stress after subarachnoid hemorrhage: a rodent model study.Annals of medicine · 2026Article
- The role of Nrf2 and PPARgamma in the improvement of oxidative stress in hypertension and cardiovascular diseases.Physiological research · 2020Review
- Astaxanthin Prevents Decreases in Superoxide Dismutase 2 Level and Superoxide Dismutase Activity inJournal of cancer prevention · 2019Article
- AMP-Activated Protein Kinase as a Reprogramming Strategy for Hypertension and Kidney Disease of Developmental Origin.International journal of molecular sciences · 2018Review
- Interplay between the renin-angiotensin system, the canonical WNT/β-catenin pathway and PPARγ in hypertension.Current hypertension reports · 2018Review
- The Effect of Chronic NO Synthase Inhibition on the Vasoactive and Structural Properties of Thoracic Aorta, NO Synthase Activity, and Oxidative Stress Biomarkers in Young SHR.Oxidative medicine and cellular longevity · 2018Article
- Age-dependent redox status in the brain stem of NO-deficient hypertensive rats.Journal of biomedical science · 2017Article
- Paradoxical Inhibition of Glycolysis by Pioglitazone Opposes the Mitochondriopathy Caused by AIF Deficiency.EBioMedicine · 2017Article
- Alternative Interventions to Prevent Oxidative Damage following Ischemia/Reperfusion.Oxidative medicine and cellular longevity · 2016Review
- Article
- PPARs Link Early Life Nutritional Insults to Later Programmed Hypertension and Metabolic Syndrome.International journal of molecular sciences · 2015Review
- Activation of central PPAR-γ attenuates angiotensin II-induced hypertension.Hypertension (Dallas, Tex. : 1979) · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
PPAR γ receptor plays an important role in oxidative stress response. Its agonists can influence vascular contractility in experimental hypertension. Our study was focused on the effects of a PPAR γ agonist pioglitazone (PIO) on blood pressure regulation, vasoactivity of vessels, and redox-sensitive signaling at the central (brainstem, BS) and peripheral (left ventricle, LV) levels in young prehypertensive rats. 5-week-old SHR were treated either with PIO (10 mg/kg/day, 2 weeks) or with saline using gastric gavage. Administration of PIO significantly slowed down blood pressure increase and improved lipid profile and aortic relaxation after insulin stimulation. A significant increase in PPAR γ expression was found only in BS, not in LV. PIO treatment did not influence NOS changes, but had tissue-dependent effect on SOD regulation and increased SOD activity, observed in LV. The treatment with PIO differentially affected also the levels of other intracellular signaling components: Akt kinase increased in the the BS, while β -catenin level was down-regulated in the BS and up-regulated in the LV. We found that the lowering of blood pressure in young SHR can be connected with insulin sensitivity of vessels and that β -catenin and SOD levels are important agents mediating PIO effects in the BS and LV.
Identifiers
What OpenQuestion holds
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.