Thiago Bruder do Nascimento, PhD
- Assistant Professor of Pediatrics
- Member, Vascular Medicine Institute (VMI), University of Pittsburgh School of Medicine
The Bruder Lab focuses in understanding the physiological and pathophysiological mechanisms whereby vascular injury occurs in hypertension, metabolic diseases, and Kawasaki’s disease. The lab is trying to decipher the connection between adipose tissue and vascular homeostasis by studying the effects of different adipose tissue-derived bioactive products, so called adipokines, on vascular function, inflammation, and blood pressure control. The major goal of his lab is to decipher new pharmacological targets to protect the vasculature from injuries, subsequently minimizing end-organ damage. Bruder Lab uses an integrative approach, consisting of state-of-the-art techniques to measure blood pressure and vascular function, as well as a wide range of physiological, pharmacological, and molecular methods, which involve in vitro, ex vivo, and in vivo studies. The laboratory has been using genetically engineered and induced mouse models of obesity, lipodystrophy, hypertension, and Kawasaki’s disease.
Professional and Scientific Society Memberships
- Americal Physiological Society, 2014-current
- American Society for Pharmacology and Experimental Therapeutics, 2014-2015
- American Heart Association, 2015-current
Education & Training
- BS, Physical Education, Integrated University of Botucatu, 2008
- BS, Cardiovascular Pharmacology, University of Sao Paulo State, 2008
- MS, Cardiovascular Pharmacology, University of Sao Paulo State, 2011
- PhD, Cardiovascular Pharmacology, University of Sao Paulo State, 2014
- Postdoctoral Fellow, Georgia Regents University, 2014-2015
- Instructor, University of Sao Paulo, 2015-2016
- Postdoctoral Fellow, Augusta University, 2016-2019
Bruder-Nascimento T, Chinnasamy P, Riascos-Bernal DF, Cau SB, Callera GE, Touyz RM, Tostes RC, Sibinga NE. Angiotensin II induces Fat1 expression/activation and vascular smooth muscle cell migration via Nox1 dependent reactive oxygen species generation. J Mol Cell Cardiol. 2014; 66:18-26.
Bruder-Nascimento T, Callera GE, Montezano AC, He Y, Antunes TT, Cat AN, Tostes RC, Touyz RM. Vascular injury in diabetic db/db mice is ameliorated by atorvastatin: role of Rac1/2-sensitive Nox-dependent pathways. Clin Sci (Lond). 2015; 128(7):411-23.
Bruder-Nascimento T, Kennard S, Antonova G, Mintz JD, Bence KK, Belin de Chantemèle EJ. Deletion of Ptp1b in pro-opiomelanocortin neurons increases energy expenditure and impairs endothelial function via TNF-α dependent mechanisms. Clin Sci (Lond). 2016 1;130(11):881-93.
Bruder-Nascimento T, Ferreira NS, Zanotto CZ, Ramalho F, Pequeno IO, Olivon VC, Neves KB, Alves-Lopes R, Campos E, Silva CA, Fazan R, Carlos D, Mestriner FL, Prado D, Pereira FV, Braga T, Luiz JP, Cau SB, Elias PC, Moreira AC, Câmara NO, Zamboni DS, Alves-Filho JC, Tostes RC. NLRP3 Inflammasome Mediates Aldosterone-Induced Vascular Damage. Circulation. 2016 6;134(23):1866-1880.
Bruder-Nascimento T, Kennard S, Faulkner JL, Antonova G, Patel VS, Fulton DF, Chen W, Belin de Chantemèle EJ. Leptin restores endothelial function and vascular adrenergic contractility in a mouse model of congenital generalized lipodystrophy (CGL). Hypertension. 2019 74 (6), 1399-1408.
Bruder-Nascimento T, Kress T, Kennard S, Belin de Chantemele, EJ. HIV Protease Inhibitor Ritonavir Impairs Endothelial Function Via Reduction in Adipose Mass and Endothelial Leptin Receptor-Dependent Increases in NADPH Oxidase 1 (Nox1), C-C Chemokine Receptor Type 5 (CCR5), and Inflammation. J Am Heart Assoc 2020 20;9(19): e018074.
Cau SB, Bruder-Nascimento A, Silva MB, Ramalho FNZ, Mestriner F, Rheure Alves-Lopes R, Ferreira N, Tostes RC, Bruder-Nascimento T. Angiotensin-II activates vascular inflammasome and induces vascular damage. Vascular Pharmacology. 2021 Jun 4:106881
Academic and Research Interests
- Vascular Biology
- Blood Pressure
- Cardiovascular Disease
- Kawasaki's Disease
Career Development Award-AHA857268 Progranulin on Kawasaki's disease -induced vascular damage 2021-2024
R00 HL140139-03 Leptin, a therapeutic avenue for the treatment of vascular disease, focus on congenital and antiretroviral therapy-associated lipodystrophies, 2019-2022