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Rossella Menghini

Researcher at University of Rome Tor Vergata

Publications -  70
Citations -  8636

Rossella Menghini is an academic researcher from University of Rome Tor Vergata. The author has contributed to research in topics: Insulin resistance & Insulin. The author has an hindex of 28, co-authored 67 publications receiving 7803 citations.

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Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 - 
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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MicroRNA 217 Modulates Endothelial Cell Senescence via Silent Information Regulator 1

TL;DR: The data pinpoint miR-217 as an endogenous inhibitor of SirT1, which promotes endothelial senescence and is potentially amenable to therapeutic manipulation for prevention of endothelial dysfunction in metabolic disorders.
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Insulin-Dependent Activation of Endothelial Nitric Oxide Synthase Is Impaired by O-Linked Glycosylation Modification of Signaling Proteins in Human Coronary Endothelial Cells

TL;DR: The data show that hyperglycemia impairs activation of the IR/IRS/PI3-K/Akt pathway, resulting in deregulation of eNOS activity, and carotid plaques from type 2 diabetic patients showed increased endothelial O-GlcNAcylation with respect to nondiabetics.
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MiR-146a is modulated in human endothelial cell with aging

TL;DR: A miR-146a is identified that is progressively modulated in endothelial cells with aging and involved in a premature senescence-like phenotype through direct targeting of the NOX4 protein, implicated in cellsenescence and aging.
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Timp3 deficiency in insulin receptor–haploinsufficient mice promotes diabetes and vascular inflammation via increased TNF-α

TL;DR: A novel interaction between insulin action and control of inflammation is reported, resulting in glucose intolerance and vascular inflammation and amenable to therapeutic modulation, suggesting that an interplay between reduced insulinaction and unchecked TACE activity promotes diabetes and vascularinflammation.