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Relevant bibliographies by topics / HCC, In-stent Restenosis, cell-proliferation,siRNA

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Journal articles
Dissertations / Theses

Academic literature on the topic 'HCC, In-stent Restenosis, cell-proliferation,siRNA'

Author: Grafiati

Published: 11 March 2023

Last updated: 31 July 2025

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Journal articles on the topic "HCC, In-stent Restenosis, cell-proliferation,siRNA"

1

Thiel, William H., Thomas Bair, Andrew S. Peek, et al. "Abstract 18955: VSMC-Targeted Aptamer-siRNA Chimeras as Inhibitors of Intimal Hyperplasia." Circulation 126, suppl_21 (2012). http://dx.doi.org/10.1161/circ.126.suppl_21.a18955.

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Arterial revascularization by stenting is associated with restenosis due to proliferation of vascular smooth muscle cells (VSMCs) and intimal hyperplasia. Although the use of cell cycle inhibitors in drug eluting stents (DES) has reduced the rate of in-stent restenosis, this approach also inhibits re-endothelialization, thereby requiring prolonged antithrombotic regimens to prevent stent thrombosis. Delivery of nucleic acid aptamers by DES is a potential novel approach due to their high specific binding affinity and potential for modification by medicinal chemistry. The goal of this study was

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2

Simard, Trevor, Richard Jung, Pietro Di Santo, et al. "Dipyridamole and vascular healing following stent implantation." Frontiers in Cardiovascular Medicine 10 (September 8, 2023). http://dx.doi.org/10.3389/fcvm.2023.1130304.

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IntroductionPatients undergoing coronary stent implantation incur a 2% annual rate of adverse events, largely driven by in-stent restenosis (ISR) due to neointimal (NI) tissue proliferation, a process in which smooth muscle cell (SMC) biology may play a central role. Dipyridamole (DP) is an approved therapeutic agent with data supporting improved vascular patency rates. Pre-clinical data supports that DP may enact its vasculoprotective effects via adenosine receptor-A2B (ADOR-A2B). We sought to evaluate the efficacy of DP to mitigate ISR in a pre-clinical rabbit stent model.Methods &amp; R

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Santiago, Fernando S., Yue Li, Ling Zhong, Mark J. Raftery, Laurence Lins, and Levon M. Khachigian. "Truncated YY1 interacts with BASP1 through a 339KLK341 motif in YY1 and suppresses vascular smooth muscle cell growth and intimal hyperplasia after vascular injury." Cardiovascular Research, January 28, 2021. http://dx.doi.org/10.1093/cvr/cvab021.

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Abstract Aims In-stent restenosis and late stent thrombosis are complications associated with the use of metallic and drug-coated stents. Strategies that inhibit vascular smooth muscle cell (SMC) proliferation without affecting endothelial cell (EC) growth would be helpful in reducing complications arising from percutaneous interventions. SMC hyperplasia is also a pathologic feature of graft stenosis and fistula failure. Our group previously showed that forced expression of the injury-inducible zinc finger (ZNF) transcription factor, yin yang-1 (YY1), comprising 414 residues inhibits neointima

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Kahles, Florian, Michael Lehrke, Anna Makowska, et al. "Abstract 547: PDE4 Inhibition Protects Against Neointimal Hyperplasia and Diminishes VCAM-1 Expression and Histone Methylation Through an Epac-Dependent Pathway." Arteriosclerosis, Thrombosis, and Vascular Biology 34, suppl_1 (2014). http://dx.doi.org/10.1161/atvb.34.suppl_1.547.

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Introduction: Upregulation of phosphodiesterase 4 (PDE4) activity causes cAMP-dependent vascular smooth muscle cell (VSMC) activation at sites of vascular inflammation and tissue remodeling. Hypothesis: PDE4 inhibition reduces VSMC activation and neointima formation following vascular injury. Methods: C57BL/6 mice (n=16) treated with roflumilast underwent guide wire-induced endothelial denudation injury of the femoral artery. Neointima formation was quantified after 4 weeks. In vitro, we analyzed the effects of roflumilast on VSMC proliferation and inflammation. Results: Roflumilast treatment

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Dissertations / Theses on the topic "HCC, In-stent Restenosis, cell-proliferation,siRNA"

1

Farra, Rossella. "siRNAs targeted against cell cycle related genes as tools to down regulate cell-proliferation in hepatocellular carcinoma and vascular smooth muscle cells." Doctoral thesis, Università degli studi di Trieste, 2008. http://hdl.handle.net/10077/2651.

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2006/2007<br>ABSTRACT Exuberant and non-controlled cellular proliferation underlines the ethio-pathogenesis of many human pathological conditions, including tumour and non-tumour diseases. Thus, the possibility to control this complex process can be extremely useful in terms of prevention/control of disease progression, especially in the light of the limited efficacy of current therapeutic approaches. In this project we draw our attention on the down regulation of cell proliferation in the context of two human diseases, namely hepatocellular carcinoma (HCC), as an example of tumour patholog

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