Faculty Member Profile

Marcela Sorelli Carneiro Ramos

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School:CCNH
Email:marcela.ramos@ufabc.edu.br
Profile:Cardiac remodeling occurs primarily as an adaptive response to an increase in demand, commonly resulting in the so called cardiac hypertrophy. The heart is a target organ in many regulatory systems, such as hormones, neuronal and hemodynamic factors, which modulate heart trophism direct or indirectly. Besides these actions, largely described in the literature, it is well known the heart is also a target of the immunological system and that some cardiovascular diseases (CVD) are preceded by general inflammation or even local response, contributing directly to remodeling or trophism alteration in this organ. The renal lesion, acute or chronic, is a highly complex pathology, and not yet completely understood. It is however, considered an inflammatory disease, highlighting contributions of endothelial lesion, leukocytes infiltration and inflammatory cytokines secretion by renal tubular cells, which may, depending on the scenario, reach other organs, namely: lungs, liver and heart. Concerning the heart, the comprehension of this systemic inflammatory response is scarce. In this work, we hypothesized that acute renal lesion dependent systemic inflammation can be deleterious to cardiac trophism, being able to impair cellular growth and possibly tissue fibrosis, acting trough pro-inflammatory cytokines. Therefore, our starting goal is to evaluate the inflammatory profile in the cardiac tissue of mice submitted to acute renal lesion induced by ischemia and reperfusion. Furthermore, we intend to study the mechanisms involved in inflammatory response modulation over cardiac trophism. This preliminary study will allow us to delineate further strategies to dissect the molecular basis of this phenomenon. We hope that this study could shed some light in this subject, resulting in the benefit of patients suffering of renal failure worldwide.
Research Areas: Impact of inflammatory response induced by ischemic renal injury on cardiac trophism; Contribution of the complement system in the modulation of cardiac hypertrophy induced by ischemic renal damage; Role of oxidative stress in cardiac hypertrophy induced by ischemic renal injury; Contribution of apoptosis in the modulation of cardiac trophism induced by ischemic renal injury
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Biosystems
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Bachelor in Science and Technology
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