The overall research goal at the Laboratory of Genetics and Molecular Cardiology is to improve the predictive and regenerative capacity in cardiovascular medicine.

We use a translational approach to:

  1. Elucidate the mechanotransduction of physical factors in the cardiovascular system;
  2. Identify the genetic determinants of complex cardiovascular phenotypes;
  3. Develop novel algorithms to predict risk and outcomes of cardiovascular diseases;
  4. Develop novel therapeutic approaches for cardiac repair.

Ongoing Projects


Adriana Castello Costa Girardi

2014 - Present Dipeptidil peptidase IV como um potencial alvo para a terapia da insuficiência cardíaca
Description: Auxílio Regular à Pesquisa FAPESP 2013/10619-8.
Members: Undergraduate (2), Academic Master (1), Doctorate (1),
2013 - Present Collaborative effort to determine the molecular bases of the blood pressure lowering effect of the incretin hormone GLP-1
Description: Pesquisa colaborativa com a University of Southern California
Members: Doctorate (2),
2012 - Present Molecular mechanisms of regulation of the proximal tubular function in hypertension
Description: Auxílio à Pesquisa FAPESP Individual 2012/10146-0

Alexandre da Costa Pereira

Ayumi Miyakawa

2000 - Present Identificação de genes com expressão diferenciada em veia safena submetida ao regime arterial
Description: The aortocoronary saphenous vein graft is the most commonly surgical procedure for revascularization of ischemic heart. Although the effective treatment of this surgical intervention, saphenous vein grafting is limited by the accelerated atherosclerosis that develops within the vein conduit. The vein graft is subjected to increased tensile stress and the adaptive vein response to the arterial hemodynamic condition may predispose to bypass occlusion. In this work, we are investigating the early molecular changes occurring in saphenous vein cultured under arterial conditions. Using an ex vivo organ culture, human saphenous vein is cultured either under venous hemodynamic condition (flow: 5 mL/min; no pressure) or arterial hemodynamic condition (flow: 50 mL/min; pressure: 80 mmHg) and the expression profile is evaluated by cDNA microarray. We also developed a vein arterialization model in rat to validate the selected target and understand molecular mechanism of vein graft disease.
Members: Doctorate (2),

Jose Eduardo Krieger

Luís Henrique Wolff Gowdak

Miriam Helena Fonseca Alaniz

2012 - Present Beta-arrestin-mediated signal transduction involvement in the anti-apoptotic effect of laminar shear stress in vascular endothelial cells.
Description: The blood vessels are continuously exposed to hemodynamic forces that regulate physiological and pathological aspects of the circulatory system. The endothelial cell acts as a sensor of the hemodynamic forces and high intensity laminar shear stress protects against the development of atherosclerosis by modulating the phenotype and function of vascular endothelium. Although the exact mechanisms have not been fully elucidated, several membrane molecules and intracellular signaling pathways are involved in mechanotransduction to shear stress. Recently it has been shown that apart from acting on the desensitization and internalization of the G protein-coupled receptors, beta-arrestins modulate various intracellular signaling pathways. Some of cellular effects mediated by beta arrestins include processes such as chemotaxis, apoptosis and cell proliferation; they are induced by different agents, and may contribute to endothelial dysfunction and the development of atherosclerotic lesions. Preliminary data from our group suggest the involvement of beta-arrestins mediated signal transduction in shear stress induced production of nitric oxide in endothelial cells. Thus, considering the processes mediated by beta- arrestins and the effects promoted by shear stress, in this project we propose to investigate the involvement of intracellular signaling pathway mediated by beta- arrestins 1 and 2 in the anti-apoptotic responses induced by laminar shear stress in endothelial cells. For this purpose, primary culture of human umbilical vein endothelial cells (HUVEC) will be transfected with siRNA against the isoforms 1 and 2 of beta-arrestins and subjected to a chronic laminar shear stress. It will be analyzed the nitric oxide production, apoptosis rate and signaling pathways. These findings will establish a key role for beta-arrestin in mediating cellular cytoprotective functions and define the biochemical pathways mediating this regulation.
Members: Undergraduate (1), Doctorate (1),