Cardiovascular diseases (CVD) are the cause of much of the deaths, due not only to genetic factors, but also to environmental factors, due to the modern way of life. However, they may be secondary to other diseases, such as cardiorenal syndromes (SCRs). Cardiorenal syndromes are diseases that show the intense connection between the functioning of the kidneys and the heart and are subdivided into five categories. Cardiorenal Syndrome type 3 (SCR 3) is characterized by renal injury that triggers damage to cardiac tissue. One of the lesions that can generate this type of disease is acute renal injury, as is the case of ischemia and reperfusion injury, very common in hemorrhagic shocks and kidney transplants. Although many factors compose the pathophysiology of this syndrome, our laboratory has already identified the great relevance of the immune system and oxidative stress in cardiac changes induced by ischemic renal injury. In this sense, the immune system, through the pro-inflammatory cytokines IL-6 and IL-1², promotes cardiac structural alterations such as cardiac hypertrophy, in addition to electrical changes induced by ischemic renal injury. Considering that: I) the cellular and molecular mechanisms involved in the development of SCR 3 are not yet fully understood and II) the oxidative stress generated by the imbalance between oxidant components and antioxidants generated in ischemia injury is an important component in the modulation of renal and cardiac functions; the present study aims to evaluate the role of oxidative stress in cardiac changes induced by renal ischemia. To do so, we will use models of renal cell culture that will be submitted to hypoxia and, subsequently, we will perform the treatment of cardiomyocytes submitted to the culture medium conditioned by renal cells previously submitted to hypoxia. The molecular parameters related to cardiac trophism, as well as parameters related to inflammatory status and redox balance, will be evaluated. The purpose of the in vitro experiments is to characterize the cellular mechanisms involved in the development of SCR 3, previously established in our laboratory studies, using in vivo models.
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