Adipokines, ageing, and vascular damage

The main physiologic function of adipokines on the energy metabolism and cardiovascular homeostasis, among others, are well known. In last years, our laboratory is providing increasing evidence about possible role as mediators vascular damage, by inducing different pro-inflammatory pro-senescent mechanisms. secretion like visfatin or dipeptidylpeptidase-4 (DPP4) adipose tissue, particularly visceral fat, enhanced in obese type 2 diabetic patients. Both enzymes metabolically active that can induce activation specific receptors, namely 4 “toll receptors” (TLR4) for “protease activated receptor 2” (PAR2) DPP4. Stimulation such receptors triggering known mechanisms, nuclear transcription factor-κB (NF-κB) inflammasome NLRP3 (“nucleotide-binding, leucine-rich-repeat, pyrin domain containing 3”), a cell structure transforms immature forms classic cytokines their derivates, interleukin-1β (IL-1β) interleukin 18 (IL-18). It worth to note these final effectors harmful effects its blockade be very relevant therapeutic approach. experiments, antagonism IL-1 with anakinra prevents inflammatory senescent evoked Moreover, this finding agreement data from other researchers, results CANTOS clinical trial, which demonstrate important cardioprotective effect mediated anti-inflammatory monoclonal antibody canakinumab. On hand, we have also provided experimental vasculopotective adipokines, angiotensin-(1-7), able induce, through Mas expression klotho protein antioxidant pathways, Nrf2-HO-1 (“nuclear factor erythroid-2 y hemoygenase-1”).