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Contribution of autophagic processes in perivascular adipose tissue hyperinflammation associated with metabolic syndrome

Grant number: 21/08847-9
Support Opportunities:Scholarships in Brazil - Post-Doctorate
Effective date (Start): January 01, 2022
Field of knowledge:Biological Sciences - Pharmacology - Cardiorenal Pharmacology
Principal Investigator:Rita de Cassia Aleixo Tostes Passaglia
Grantee:Rafael Menezes da Costa
Host 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):22/06639-2 - The role of beclin 1-dependent autophagy in aldosterone-induced perivascular adipose tissue dysfunction, BE.EP.PD


Metabolic syndrome triggers structural and functional changes in Perivascular Adipose Tissue (PVAT), leading to an imbalance in the production and release of PVAT-derived vasodilator factors, in favor of vasoconstrictor and pro-inflammatory factors, as well as changes in activated signaling pathways by these factors in vascular cells. An important mechanism proposed to explain the loss of the anticontractile effect of PVAT in metabolic syndrome is the participation of inflammatory mediators. Autophagic processes are extremely important for inflammatory tolerance in tissues compromised by metabolic diseases. Autophagy is critical for the secretion of anti-inflammatory cytokines by macrophages in response to phagocytosis of apoptotic cells. Defects in autophagy processes, canonical and non-canonical, alter the elimination of dead cells by macrophages, inducing the development of a local autoimmune syndrome. In this sense, macrophages start to express pro-inflammatory genes and trigger the production of interferon, resulting in the recruitment of T lymphocytes and consequent amplification of the inflammatory environment. Thus, this research proposal intends to elucidate the mechanisms involved in the control of macrophage activation during autophagic processes in the PVAT of individuals with metabolic syndrome. Furthermore, revealing the function of the autophagic components of macrophages can justify the genesis of PVAT inflammation, as well as justify the vascular damage associated with the metabolic syndrome. To investigate all these aspects, proteome assay approaches, TurboID screening, Cre system and vascular function study techniques will be used. (AU)

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