Cardiovascular diseases (CVD) are the leading cause of mortality in developed countries. Pathological processes in the heart are associated with the differential expression profile of genes known to be important for cardiac function. Current understanding of cardiac gene expression shows that transcriptional regulation is the primary regulator, where transcription factors bind to enhancer/promoter regulatory sequences to activate gene expression. Nuclear factor κB (NFκB) is one of the main transcription factors activating the expression of genes whose products play a key role in the development of cardiovascular pathologies and inflammatory and/or viral diseases [20]. NF-kB is a redox-sensitive transcription factor present in most cell types with a common p50/65 heterodimer. Inactive NF-kB dimers bind to inhibitors of NF-kB (IkB) proteins and remain in the cytosol. Stimuli, such as reactive oxygen species (ROS) and other inflammatory factors, may play a role in NF-κB activation (20). Excessive activation of NF-κB has been implicated in human inflammatory diseases, such as atherosclerosis. Due to the widespread involvement of NF-κB signaling in human pathologies, continued efforts have been made to develop inhibitors of this pathway [21]. Reports suggest that the processes of inflammation and angiogenesis are linked. Newly formed blood vessels participate in the continued recruitment of inflammatory cells, leading to the release of a variety of cytokines and growth factors promoting angiogenesis. A series of positive feedback loops creates a vicious cycle that increases inflammation, turning it into a chronic process. This concept of reciprocity also includes oxidative stress, which leads to chronic inflammation in the middle of the article...... DM [39].SIRT1 is an NAD-dependent deacetylase involved in the regulation of stress response pathways . SIRT1 modulates metabolism and hypoxic responses by deacetylating transcription factors and cofactors in pathways involved in cardiovascular diseases and cancer metabolic diseases, so the regulation of SIRT1 has received much attention ( 40 ). Expression of miR-34a in the heart and spleen is higher in older mice than in younger mice. SIRT1 expression decreased with age. Data suggest that miR-34a regulates endothelial senescence. It also inhibits EPC-mediated angiogenesis through induction of senescence [40] . MiR-34a also modulates FoxO1, a downstream target of senescence enhancing SIRT1. MiR-34a targets SIRT1 and contributes to ESC pluripotency. Thus, SIRT1 plays an important role in the cardiovascular system and miR-34a in turn modulates SIRT expression1. [41].