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Impact of inflammatory response induced by acute renal ischemia in cardiac tissue

Abstract

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. (AU)

Scientific publications
(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)
CAIO-SILVA, WELLINGTON; DA SILVA DIAS, DANIELLE; JUNHO, CAROLINA VICTORIA CRUZ; PANICO, KARINE; NERES-SANTOS, RAQUEL SILVA; PELEGRINO, MILENA TREVISAN; PIERETTI, JOANA CLAUDIO; SEABRA, AMEDEA BAROZZI; DE ANGELIS, KATIA; CARNEIRO-RAMOS, MARCELA SORELLI. Characterization of the Oxidative Stress in Renal Ischemia/Reperfusion-Induced Cardiorenal Syndrome Type 3. BIOMED RESEARCH INTERNATIONAL, v. 2020, OCT 9 2020. Web of Science Citations: 0.
JUNHO, CAROLINA VICTORIA CRUZ; CAIO-SILVA, WELLINGTON; TRENTIN-SONODA, MAYRA; CARNEIRO-RAMOS, MARCELA SORELLI. An Overview of the Role of Calcium/Calmodulin-Dependent Protein Kinase in Cardiorenal Syndrome. FRONTIERS IN PHYSIOLOGY, v. 11, JUL 14 2020. Web of Science Citations: 0.
LOPEZ ALARCON, MARIA MICAELA; TRENTIN-SONODA, MAYRA; PANICO, KARINE; SCHLEIER, YGOR; DUQUE, THABATA; MORENO-LOAIZA, OSCAR; DE YURRE, AINHOA RODRIGUEZ; FERREIRA, FABIANNO; CAIO-SILVA, WELLINGTON; COURY, PEDROSA ROBERTO; PAIVA, CLAUDIA N.; MEDEI, EMILIANO; CARNEIRO-RAMOS, MARCELA SORELLI. Cardiac arrhythmias after renal I/R depend on IL-1 beta. JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, v. 131, p. 101-111, JUN 2019. Web of Science Citations: 1.

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