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Thiago Bruder do Nascimento, PhD

  • Assistant Professor of Pediatrics
  • Member, Center for Pediatric Research in Obesity & Metabolism (CPROM)
  • Member, Vascular Medicine Institute (VMI), University of Pittsburgh School of Medicine
  • Member, Richard King Mellon Foundation Institute for Pediatric Research

Thiago Bruder do Nascimento, PhD, joined the Center for Pediatric Research in Obesity and Metabolism (CPROM), Department of Pediatrics, University of Pittsburgh School of Medicine, as a tenure-track assistant professor in 2019. He is interested in understanding the molecular mechanisms whereby metabolic diseases such as obesity, diabetes and lipodystrophy, lead to cardiovascular disease. More specifically, he is interested in determining the contribution of hormones secreted by adipose tissue (adipokines) to vascular biology and genesis of hypertension. 

Dr. Bruder has extensive training in vascular biology, focusing on reactive oxygen species and vascular inflammation. A major focus of his research is to understand how inflammatory response leads to cardiovascular diseases associated with metabolic diseases. As part of CPROM, his goal is to conduct a close collaboration with physicians and involve an integrative approach consisting of a wide range of physiological, pharmacological and molecular methods, and involving genetically engineered mouse models of disease. 

Dr. Bruder’s research is funded by American Heart Association (AHA) and the National Institutes of Health through a K99/R00 grant that seeks to understand the cardiovascular and metabolic functions in different metabolic disorders. His work has resulted in several peer-reviewed publications and awards from American Physiological Society and AHA. 

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

Selected Publications

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, Butler BR, Herren DJ, Brands MW, Bence KK, Belin de Chantemèle EJ. Deletion of protein tyrosine phosphatase 1b in proopiomelanocortin neurons reduces neurogenic control of blood pressure and protects mice from leptin- and sympatho-mediated hypertension. Pharmacol Res. 2015;102:235-44. 

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. 

Full Publication List via NIH PubMed

Research Interest Summary

We focus in the underlying mechanisms in the cardiovascular risk associated with metabolic diseases such as obesity, diabetes, lipodystrophy in order to decipher new pharmacological targets and minimize organ damage.

Research Interests

Leptin replacement therapy to treat vascular disease associated with lipodystrophy. 

Inflammasome regulates the vascular smooth muscle cells phenotype. 

CCL5/RANTES controls the vascular function 

Research Grants

4 R00 HL140139-03, Leptin, a therapeutic avenue for the treatment of vascular disease, focus on congenital and antiretroviral therapy-associated lipodystrophies, (PI, 85% effort), 2019-2022, $747,000

K99 HL140139-01, Leptin, a therapeutic avenue for the treatment of vascular disease, focus on congenital and antiretroviral therapy-associated lipodystrophies, (PI, 100% effort), 2018-2019, $115,506

18CDA34110202AHA,Vascular inflammation in lipodystrophy, (PI, 100% effort), 2018-relinquished in order to accept K99, $254,000

17POST33410363AHA, Leptin in lipodystrophy-associated cardiovascular disease, (PI, 100%), 2017-2018, $102,550