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Paula Reventun

Researcher at University of Alcalá

Publications -  15
Citations -  252

Paula Reventun is an academic researcher from University of Alcalá. The author has contributed to research in topics: Medicine & Enos. The author has an hindex of 6, co-authored 10 publications receiving 147 citations. Previous affiliations of Paula Reventun include Johns Hopkins University & Universidad Francisco de Vitoria.

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Oral administration of bisphenol A induces high blood pressure through angiotensin II/CaMKII-dependent uncoupling of eNOS

TL;DR: Oral administration of bisphenol A induces high blood pressure through angiotensin II/CaMKII‐dependent uncoupling of eNOS, which suggests that AngII uncouples eN OS and contributes to the BPA‐induced endothelial dysfunction by promoting oxidative and nitrosative stress.
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Bisphenol A induces coronary endothelial cell necroptosis by activating RIP3/CamKII dependent pathway.

TL;DR: The results reveal a novel pathogenic role of BPA on the coronary circulation and induces endothelial cell necroptosis, promotes the weakening of coronary vascular wall, which caused internal ventricular hemorrhages, delaying the reparative process and ultimately leading to cardiac dysfunction.
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EMMPRIN-Targeted Magnetic Nanoparticles for In Vivo Visualization and Regression of Acute Myocardial Infarction.

TL;DR: Injection of NAP9 at the time of or one day after IR, was enough to reduce progression of myocardial cell death when compared to Control and NAPSC injected mice and EMMPRIN targeted nanoparticles as a new approach to the mitigation of ischemic/reperfusion injury.
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iNOS-Derived Nitric Oxide Induces Integrin-Linked Kinase Endocytic Lysosome-Mediated Degradation in the Vascular Endothelium

TL;DR: Endocytosis regulates ILK signaling in vascular remodeling where there is an overload of inducible NO, and thus its inhibition may represent a novel target to fight atherosclerotic disease.
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Bisphenol A impaired cell adhesion by altering the expression of adhesion and cytoskeleton proteins on human podocytes.

TL;DR: Data show that BPA induced a novel type of podocytopathy characterizes by an impairment of podocyte adhesion, by altering the expression of adhesion and cytoskeleton proteins, which provide a mechanism by which BPA could participate in the pathogenesis and progression of renal diseases.