ArticleBMC neurology2019
PPAR-γ promotes p38 MAP kinase-mediated endothelial cell permeability through activating Sirt3.
Article in BMC neurology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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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.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- Uncovering the metabolic-epigenetic links between gene expression and stroke: insights from lactylation pathway MR study.Neurological research and practice · 2026Article
- Astragaloside IV inhibits the progression of hypertensive heart disease via the RXRA/PPARG/SIRT3 axis.Journal of molecular medicine (Berlin, Germany) · 2025Article
- Article
- Chrysin Attenuates Myocardial Cell Apoptosis in Mice.Cardiovascular toxicology · 2025Article
- Sirtuins: Promising Therapeutic Targets to Treat Ischemic Stroke.Biomolecules · 2023Review
- Article
- A Promising Strategy to Treat Neurodegenerative Diseases by SIRT3 Activation.International journal of molecular sciences · 2023Review
- SIRT3 inhibitor 3-TYP exacerbates thioacetamide-induced hepatic injury in mice.Frontiers in physiology · 2022Article
- Angiotensin II Induces Cardiac Edema and Hypertrophic Remodeling through Lymphatic-Dependent Mechanisms.Oxidative medicine and cellular longevity · 2022Article
- Hyperglycemic Condition Causes Pro-Inflammatory and Permeability Alterations Associated with Monocyte Recruitment and Deregulated NFκB/PPARγ Pathways on Cerebral Endothelial Cells: Evidence for Polyphenols Uptake and Protective Effect.International journal of molecular sciences · 2021Article
- CXCL6 regulates cell permeability, proliferation, and apoptosis after ischemia-reperfusion injury by modulating Sirt3 expression via AKT/FOXO3a activation.Cancer biology & therapy · 2021Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
backgroundIschemia-reperfusion (I/R)-induced vascular dysfunction is the main factor to acute ischemic stroke. Sirt3 is one of the sirtuin family members, which plays an important role in the development of neurological diseases.
methodsIn this study, we constructed I/R injury model on HBMEC cells and induced the overexpression of Sirt3 in model cells. Meanwhile, the p38 activator U-46619 was used to examine the connection between Sirt3 and p38. We also examined the level of endothelial associated proteins, including occluding, ZO-1 and claudin-4 by using qRT-PCR and western blot.
resultsOur findings indicated that overexpression of Sirt3 decreased the permeability of model cells and promoted in the growth of endothelial cells. However, the activation of p38 could antagonize the function of Sirt3 in HBMEC cells. Moreover, Our results indicated a positive correlation between Sirt3 and inter-endothelial junction proteins. Importantly, PPAR-γ agonist and inhibitor were utilized to investigate the role of PPAR-γ in Sirt3 mediated cell function. Sirt3 was targeted by PPAR-γ in model cells.
conclusionsTaken together, this research not only demonstrated PPAR-γ might benefit to the growth of endothelial cell though activating Sirt3 but also indicated its potential value in the treatment for ischemic stroke.
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Registered trials
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