Scholarship 22/11975-1 - Nefrologia, Poluição do ar - BV FAPESP
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Pollution is the motor of premature ageing of the kidney

Grant number: 22/11975-1
Support Opportunities:Scholarships in Brazil - Doctorate (Direct)
Start date until: September 01, 2022
End date until: May 31, 2025
Field of knowledge:Health Sciences - Medicine - Medical Clinics
Agreement: Netherlands Organisation for Scientific Research (NWO)
Principal Investigator:Lucia da Conceição Andrade
Grantee:Antonio Carlos Parra Ferreira dos Santos
Host Institution: Faculdade de Medicina (FM). Universidade de São Paulo (USP). São Paulo , SP, Brazil
Associated research grant:19/19433-0 - Pollution is the motor of premature ageing of the kidney, AP.TEM

Abstract

Premature renal ageing is a risk factor for cardio-vascular adverse events, the development of Chronic Kidney Disease (CKD) and progression towards End Stage Renal Disease (ESRD). ESRD is associated with low quality of life, high morbidity and mortality, and tremendous health care expenses. The incidence of ESRD varies greatly among countries with 6% in The Netherlands compared to 11% in Sao Paulo. One of the neglected factors possibly underlying heterogeneity in renal ageing, is the exposure to environmental factors. Recently epidemiological studies have linked exposure to Particulate Matter in aerodynamic air (PM2.5) to an increased risk of CKD. Epigenetic changes, oxidative stress and chronic inflammation are among the mechanisms mediating the adverse health effects of PM2.5. Research into the interplay between individual exposure to PM2.5, epigenetic responses and premature renal ageing is limited. Our project will fill the gap of this knowledge. We hypothesize that exposure to PM2.5 forms an accelerator of renal ageing, enhancing the risk of CKD. To unravel the molecular and biological changes induced by PM2.5 exposure in the kidney, we will use a unique experimental model: the Harvard Ambient Particle Concentrator, in which mice will be exposed to PM2.5 during the ageing process and after the induction of renal injury. Using this setup, we will identify a unique signature of PM2.5, encompassing epigenetic, transcriptomic and metabolic changes, which will be evaluated as a risk factor for renal healthspan in observational cohorts in the Netherlands and in Sao Paulo. We envision that this signature will predict individual differences in renal function decline and will be important to adopt preventive measures to promote renal healthy ageing. Additionally, using state-of-the-art techniques, we aim at the chemical, elemental characterization and traceability of PM2.5 components in blood, kidney and urine, to unravel which elements of PM2.5 are toxic for the kidneys. (AU)

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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)
SANCHES, TALITA ROJAS; PARRA, ANTONIO CARLOS; SUN, PEIQI; GRANER, MARIANA PEREIRA; ITTO, LUCAS YUJI UMESAKI; BUTTER, LOES MARIA; CLAESSEN, NIKE; ROELOFS, JORIS J. T. H.; FLORQUIN, SANDRINE; VERAS, MARIANA MATERA; et al. Air pollution aggravates renal ischaemia-reperfusion-induced acute kidney injury. JOURNAL OF PATHOLOGY, v. 263, n. 4-5, p. 12-pg., . (19/26385-2, 16/18438-0, 18/24171-2, 19/19433-0, 22/11975-1)
DA SILVA, IGOR OLIVEIRA; DE MENEZES, NICOLE K.; JACOBINA, HELOISA D.; PARRA, ANTONIO CARLOS; SOUZA, FELIPE LIMA; CASTRO, LETICIA CARDOSO; ROELOFS, JORIS; TAMMARO, ALESSANDRA; GOMES, SAMIRAH ABREU; SANCHES, TALITA ROJAS; et al. Obesity aggravates acute kidney injury resulting from ischemia and reperfusion in mice. SCIENTIFIC REPORTS, v. 14, n. 1, p. 11-pg., . (18/23183-7, 22/11975-1, 18/23182-0, 20/12278-7)

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