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The research led by Thiago Bruder do Nascimento, PhD, examines the mechanisms that adipose tissue contributes towards cardiovascular health and disease, especially in obesity, diabetes and lipodystrophy. Adipose tissue has been shown to be a major conductor for the “cardiovascular symphony,” making it a promising therapeutic target in treating cardiovascular diseases.
According to the World Health Organization, more people die annually from cardiovascular diseases than from any other cause. Metabolic diseases such as obesity, diabetes and lipodystrophy markedly increase the cardiovascular risk, in most cases through the alteration of adiposity levels and adipocytes function. Compelling evidence on the biology and function of the adipose tissue has led to a better understanding of its role in health and disease.
Adipose tissue is now recognized as a critical regulator of cardiovascular health, via the secretion of numerous bioactive products such as the adipokines, which present a wide range of endocrine and paracrine effects on the cardiovascular system. Several diseases lead to an alteration on the profile of adipose tissue in terms of expansion, body distribution and quality, triggering a dysregulated endocrine and/or paracrine functions. Active receptors for adipokines are broadly expressed in mammalian cells, including in vascular and immune cells, which contribute to cardiovascular health and disease.
The Bruder Lab focuses in the underlying mechanisms in cardiovascular risk associated with metabolic diseases in order to decipher new pharmacological targets and minimize organ damage.
In a previous study, Dr. Bruder demonstrated that adipose tissue contributes to vascular homeostasis by producing leptin, which activates its receptor in the vascular endothelium and maintains the vascular redox balance via NADPH oxidase 1-derived reactive oxygen species. These findings created a new vascular biology concept that the endothelial leptin receptor is essential for vascular health. Based on this data, the Bruder Lab has been trying to understand which mechanisms within adipose tissue contribute to cardiovascular health and disease.
Adipocytes have the ability to produce several cytokines known as adipocytokines or adipokines (leptin, adiponectin, chemerin and others). A certain part of these adipokines can reach distant organs through systemic circulation, where they can exert a wide range of biological actions, including the regulation of food intake and body weight, insulin sensitivity, inflammation, coagulation, or vascular function and structure. The Bruder Lab is working to understand the contribution of adipokines on vascular homeostasis and genesis of hypertension focusing on vascular redox signaling and inflammation.
Dr. Bruder’s studies use an integrative approach, consisting of a wide range of physiological, pharmacological, and molecular methods, which involve in vitro, ex vivo, and in vivo studies. The laboratory has used genetically engineered and induced mouse models of obesity, diabetes, lipodystrophy, and hypertension.
Adipocytes-derived Hormones and Cardiovascular Function
Metabolic diseases such as obesity, diabetes and lipodystrophy have been associated with changes in adiposity and cardiovascular function.
The Bruder Lab
UPMC Children’s Hospital of Pittsburgh
John G. Rangos Sr. Research Center, Suite 5131
4401 Penn Avenue
Pittsburgh, PA 15224
Lab (Bay #17)
2019 – Dr. Bruder received the prestigious Stephanie Watts Career Development Award from the American Heart Association’s Council on Hypertension at the Hypertension 2019 Scientific Sessions in New Orleans. For this achievement, his lab was awarded a DSI telemetry system for blood pressure and electrocardiogram recording. As part of the Vascular Stiffness and Fibrosis section of the event, Dr. Bruder also presented his study “Leptin Restores Endothelial Function, Diminishes Vascular Adrenergic Contractility, but Does Not Alter Arterial Stiffness and Blood Pressure, in a Mouse Model of Congenital Generalized Lipodystrophy.”
Leptin Restores Endothelial Function via Endothelial PPARγ- Nox1 Mediated Mechanisms in a Mouse Model of Congenital Generalized Lipodystrophy
Bruder-Nascimento T, Faulkner JL, Haigh S, Kennard S, Antonova G, Patel VS, Fulton DR, Chen W, Belin de Chantemèle EJ
2019 Oct 28
NLRP3 Inflammasome Mediates Aldosterone-Induced Vascular Damage
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
2016 Dec 6
Ptp1b Deletion in Pro-opiomelanocortin Neurons Increases Energy Expenditure and Impairs Endothelial Function via TNF-α Dependent Mechanisms
Bruder-Nascimento T, Kennard S, Antonova G, Mintz JD, Bence KK, Belin de Chantemèle EJ
Deletion of Protein Tyrosine Phosphatase 1b in Pro-opiomelanocortin Neurons Reduces Neurogenic Control of Blood Pressure and Protects Mice From Leptin- and Sympatho-mediated Hypertension
Bruder-Nascimento T, Butler BR, Herren DJ, Brands MW, Bence KK, Belin de Chantemèle EJ
Vascular Injury in Diabetic db/db Mice is Ameliorated by Atorvastatin: Role of Rac1/2-Sensitive Nox-dependent Pathways
Bruder-Nascimento T, Callera GE, Montezano AC, He Y, Antunes TT, Nguyen Dinh Cat A, Tostes RC, Touyz RM
Angiotensin II Induces Fat1 Expression/activation and Vascular Smooth Muscle Cell Migration via Nox1-dependent Reactive Oxygen Species Generation
Bruder-Nascimento T, Chinnasamy P, Riascos-Bernal DF, Cau SB, Callera GE, Touyz RM, Tostes RC, Sibinga NE
Journal of Molecular and Cellular Cardiology
The Bruder Lab is looking for talented post-doctoral fellows, graduate and undergraduate students interested in metabolic disease, vascular biology and blood pressure regulation. Please contact Dr. Thiago Bruder do Nascimento via email if you are interested.
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