The knowledge of the molecular basis of diseases was facilitated by the advances of high throughput functional genomics, allowing deep analysis of Folinic acid calcium salt pentahydrate genome-wide results. In this sense, DNA microarray technology can be used to study a complex disease, as it offers the advantage of analyzing thousands of genes simultaneously. This technology coupled with bioinformatics tools may detect changes in genes previously unknown to participate in diseases, identifying possible altered biological functions and providing new drug targets to be investigated. Given this landscape, comparing in what way IPC and Hemin treatment can protect the kidney against IRI could be a relevant approach to analyze which mechanisms are involved in these maneuvers. Based on that, the aim of the present work was to investigate the differential gene expression patterns associated with renal IRI, IPC and Hemin treatment. In addition, gene expression profiles identified for each case were submitted to functional enrichment analysis and a comprehensive literature review was performed to map the state of the art regarding the biological functions overrepresented here. Therefore, MAPK activation can determine renal epithelial cell survival during oxidative injury, and the differences in cellular outcome of the various nephron regions may be related to specific activation of different MAPKs. Also, MAPK pathway intimately participates of the downstream signal transduction associated with innate immune response and subsequent proinflammatory cytokine production. The activity of p38 MAPK, JNK and ERK1/2, as well as several enzymes up and downstream of these pathways, is regulated by their phosphorylation status. Moreover, a complex network of negative regulatory mechanisms present in MAPK signaling prevents deleterious 4-(Benzyloxy)phenol effects of innate immune response. Part of this feedback mechanism is associated with inactivation of MAPKs by phosphatases. Notably, many MAPK signaling phosphatases were found here to be overexpressed after IRI. The important class of dual specificity phosphatases was remarkably upregulated, showing the relevance of this class of enzymes to regulate MAPK signaling in this context. Also relevant, MAPK signaling was the most upregulated functionally enriched function observed in the comparison IPC+IRI 
vs Control. Indeed, some studies have already addressed the activation of MAPK signaling by IPC and IRI. Moreover, after Hemin treatment, MAPKKK cascade was also one of the overrepresented themes. Taken these multiple lines of evidence together, one can speculate that the attenuation of renal damage effects by MAPKs is an important agenda for future research, which should be fully explored. Our functional genomics approach revealed in an integrative manner the differential transcriptome profiles and subsequent enriched biological functions among the groups, providing a global picture of how the kidney behaves after IRI. Although previous works have already addressed differential gene expression following IRI in animal models, these studies used microarray sets containing much less probes than used here. Consequently, many new relevant genes were found in our study, updating the current information regarding transcriptome regulation following IRI. Also, our findings were consistent with these previous microarray studies, confirming the participation of genes associated with apoptosis, inflammation, extracellular matrix, stress response, growth factors, adhesion molecules, proteases, etc.