Advanced search
Start date
Betweenand

Center for Research on Inflammatory Diseases - CRID

Grant number: 16/16207-1
Support type:Scholarships in Brazil - Post-Doctorate
Effective date (Start): October 01, 2016
Effective date (End): June 01, 2021
Field of knowledge:Biological Sciences - Pharmacology - Cardiorenal Pharmacology
Principal Investigator:Rita de Cassia Aleixo Tostes Passaglia
Grantee:Josiane Fernandes da Silva
Home Institution: Faculdade de Medicina de Ribeirão Preto (FMRP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil
Associated research grant:13/08216-2 - CRID - Center for Research in Inflammatory Diseases, AP.CEPID
Associated scholarship(s):17/26072-9 - Role of the redox environment and protein tyrosine phosphatase oxidation in atherosclerotic-associated processes, BE.EP.PD

Abstract

Inflammatory diseases are a complex and heterogeneous group of diseases, and an important cause of morbidity and mortality. The Center of Research on Inflammatory Diseases (CRID) intends to develop translational research in the field of inflammatory diseases. With this aim, scientists trained in molecular modelling and synthesis of molecules have been integrated to the Center and will develop new drugs to treat these diseases. The Centre's project consists of 03 subprojects: 1) infectious inflammatory diseases (leishmaniasis, Chagas disease, paracoccidioidomycosis, tuberculosis, sepsis); 2) autoimmune inflammatory diseases (rheumatoid arthritis, lupus, psoriasis, and inflammatory bowel diseases pemphigus) and allergic diseases (asthma); 3) atherosclerosis. The development of the subprojects will allow the identification of newbiological targets common to most of the above inflammatory diseases including the identification and characterization of genes playing causative roles in the disease. Atherosclerosis is a vascular disorder that leads to the most common forms of cardiovascular diseases manifested as acute coronary syndrome, myocardial infarction or stroke. For many years, atherosclerosis was considered a disease of lipid accumulation driven by diet and lifestyle. However, in the last few years this concept has changed tremendously. Currently, the underlying pathology is characterized by a chronic inflammatory process of the arterial wall that occurs at predilection sites with disturbed laminar flow. Atherosclerosis begins by endothelial dysfunction followed by adhesion of monocytes to endothelial cells, leukocytes and lipid accumulation in thevascular wall and, finally, proliferation and migration of smooth muscle cells. The focus of this subproject is to study the molecular mechanisms that affect plaque progression, the correlation between serum markers of inflammation and the plaque area as well as to identify morphological and molecular markers that discriminate between stable and vulnerable plaques. More specifically and in agreement with studies in other areas of the Center, this subproject will investigate whether factors such as the aryl hydrocarbon receptors, neutrophils extracellular traps (NETs) and glycosylation with N-acetylglucosamine (O-GlcNAc) are involved in the progression of atherosclerosis - stabilization, vulnerability and rupture of the atherosclerotic plaque. (AU)

Scientific publications
(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)
COSTA, EDUARDO D.; SILVA, JOSIANE F.; GARCIA, DANIELA C.; WAINSTEIN, ALBERTO J.; REZENDE, BRUNO A.; TOSTES, RITA C.; TEIXEIRA, MAURO M.; CORTES, STEYNER F.; LEMOS, VIRGINIA S. Decreased expression of neuronal nitric oxide synthase contributes to the endothelial dysfunction associated with cigarette smoking in human. NITRIC OXIDE-BIOLOGY AND CHEMISTRY, v. 98, p. 20-28, MAY 1 2020. Web of Science Citations: 0.
SILVA, JOSIANE FERNANDES; OLIVON, VANIA C.; MESTRINER, FABIOLA LESLIE A. C.; ZANOTTO, CAMILA ZILIOTTO; FERREIRA, RAPHAEL GOMES; FERREIRA, NATHANNE SANTOS; SILVA, CARLOS ALBERTO AGUIAR; LUIZ, JOAO PAULO MESQUITA; ALVES, JULIANO VILELA; FAZAN, RUBENS; CUNHA, FERNANDO QUEIROZ; ALVES-FILHO, JOSE CARLOS; TOSTES, RITA C. Acute Increase in O-GlcNAc Improves Survival in Mice With LPS-Induced Systemic Inflammatory Response Syndrome. FRONTIERS IN PHYSIOLOGY, v. 10, JAN 21 2020. Web of Science Citations: 0.

Please report errors in scientific publications list by writing to: cdi@fapesp.br.