| Grant number: | 09/51316-2 |
| Support Opportunities: | Regular Research Grants |
| Start date: | December 01, 2009 |
| End date: | November 30, 2011 |
| Field of knowledge: | Health Sciences - Medicine - Medical Clinics |
| Principal Investigator: | Carlos Vicente Serrano Junior |
| Grantee: | Carlos Vicente Serrano Junior |
| Host Institution: | Instituto do Coração Professor Euryclides de Jesus Zerbini (INCOR). Hospital das Clínicas da Faculdade de Medicina da USP (HCFMUSP). Secretaria da Saúde (São Paulo - Estado). São Paulo , SP, Brazil |
| City of the host institution: | São Paulo |
Abstract
LDL plays a key role in the deposition of cholesterol in the arterial wall, leading to atherosclerotic plaque formation; this process is intimately associated with induction of oxidative stress in arterial wall cells, including endothelial cells and macrophages. Oxidised LDL (oxLDL) has multiple atherogenic properties, due in part to its uptake and accumulation in macrophages. In contrast to unmodified LDL, oxLDL is taken up through scavenger receptor pathways that are not down-regulated by excess ligand and lead to the formation of macrophage foam cells, characteristic components of atherosclerotic plaques. Our recent data demonstrate that HDL particle subfractions are heterogeneous in their physiological activity. Antioxidative activity of HDL subfractions increased with increment in density, HDL2b
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