Novel Techniques, Biomarkers and Molecular Targets to Address Cardiometabolic Diseases

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  Figure 1. Pathophysiology of cardiometabolic diseases.

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  Figure 2. Major molecular targets in cardiomyocytes (a) and endothelial cells (b). By binding the corresponding microRNA (miRNA) and inhibiting this, the long noncoding RNA (lncrna) acts as a miRNA sponge and could prevent cardiomyocyte necrosis and hypertrophic growth, rescuing cardiac progenitor cell (CPC) profiling and preventing mitochondrial dysfunction. Bromodomain-containing protein 4 (BRD4) binds to RelA by recognising the acetylene-lysine residue and initiates the transcription of genes involved in the inflammatory process. The shift from oxidative phosphorylation to glycolysis is associated with mitochondrial dysfunction. In addition, the activation of glycolysis follows the activation of p300/CREB binding protein (CBP), which contributes to the recruitment of BRD4 to nucleosomes flanking transcription factor (TF) binding sites. The effect of BRD4 could be prevented by BETi inhibitors (BETi). Silent mating type information regulation 1 homologs (Sirt1) can repress the transcription of a senescence-associated secretory phenotype (SASP) through histone deacetylation. Sirt1 activity can be stimulated by an active lifestyle, healthy diet, and compounds such as resveratrol (RSV),…