Abstract
Recently, our group is developing several researches to characterize the inflammatory response in different renal diseases, by using experimental model and human samples analyses approaches. Renal diseases present an enormous socio-economic impact and a great morbid-mortality for patients. In this sense, new knowledge about their physiopathogeny that promotes better renal function outcome is necessary to improve patient survival. So far, the results obtained during these years indicate that innate and adaptive immune responses, such as endothelial cell activation, synthesis of cyclooxygenase, Bradykinin production, and CD4+ T cell are effector mechanisms of acute renal injury. However, in all studied models, it was seen that the tissue response face aggression is also relevant, and relies on expression of several so called protective genes, among them, the heme oxygenase 1 (HO-1). Besides, HO-1 being a stress-inducible protein, and its modulation can be associated to better organ function, its expression can be linked to the innate immune response toward a danger, intimately. The action of HO-1 on the innate immunity could be transferred to the adaptive part and generate nonresponsive T cells, and therefore, less tissue damage. Furthermore, here we propose to study other renal injuries than ischemia, demonstrating that this hypothesis could be applied to renal inflammatory disease in a broad sense. Finally, we hope to show that the immune response triggered by renal diseases in systemic, and could generate a positive feedback loop. In this project, we intend to study deeper the role of HO-1 in renal injuries, in different animal models and in cell culture systems. By doing that, we intend to answer our hypotheses and aims. (AU)
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