Background Recent studies have suggested that a higher body mass index (BMI) is associated with an improved prognosis in heart failure (HF). Adropin is a recently identified protein that has been implicated in the maintenance of energy homeostasis. In the present study, we investigated plasma adropin levels in patients with HF and evaluated the relationship between the levels and the severity of HF. Methods and ResultsThe study group comprised 56 patients with HF and 20 control subjects, who were divided into 4 subgroups according to New York Heart Association (NYHA) functional classification. Plasma levels of adropin, brain natriuretic peptide (BNP) and cardiac hemodynamics were determined. Plasma adropin levels were significantly increased according to the severity of NYHA class in the patients with HF; control: 6.0 ± 0.3; NYHA functional Class II: 7.6 ± 0.4; NYHA functional Class III: 9.8 ± 0.5; NYHA functional Class IV: 12.4 ± 0.6 ng/mL (p<0.01). Similarly, plasma BNP levels were significantly increased in accordance with the NYHA class. Plasma adropin levels were correlated positively with BNP (r=0.723, p< 0.001), interleukin-6 (IL-6) (r=0.326, p=0.007) and body mass index (BMI) (r=0.295, p=0.014), and negatively with left ventricular ejection fraction (LVEF) (r=-0.710, p<0.001). Conclusion Plasma adropin levels were significantly increased according to the severity of HF, and BNP and BMI had independent impact on the plasma adropin level. These findings suggest that the augmented release of adropin may be involved in the pathogenesis of HF and further study is necessary to explain the precise role of adropin in HF.

Background and Objective: Celastrol is a pentacyclic triterpenoid with a long history of therapeutic potential. Unfortunately, their prime mechanism for myocardial infarction was unknown. Therefore, the current study has investigated celastrolʼs efficiency and its cardioprotective role in isoproterenol-induced heart injury. Materials and Methods: The animals have been separated into 4 groups (n = 6). The test group was pretreated with celastrol on the 7th day at the same time as isoproterenol-induced heart damage on the 6th-7th days. The biochemical parameters were determined in serum and heart tissue homogenates. Results: Celastrol significantly decreased the myocardial infarction markers concentration in serum and increased the antioxidant concentration in isoproterenol-induced heart tissue. In addition to this, celastrol also regulates the membrane-bound as well as lysosome enzymes located in the heart tissue. Furthermore, the elevation of pro-inflammatory cytokines and NF-kB mRNA was lessened by celastrol administration. Celastrol also reduced isoproterenol-induced programmed cell death, by altering the Bcl-2, Bax and caspase-3 levels in cardiac tissue. Conclusion: Current findings suggested that administering celastrol may help to reduce cardiac damage in myocardial infarction by reducing inflammation, apoptosis and oxidative stress.

Vascular senescence is a key component in the initiation of atherosclerosis and its related cardiovascular disorders. C-X-C Motif Chemokine Ligand 12 (CXCL12), the CXC chemokine receptor 4 (CXCR4) ligand is a chemokine known to promote atherosclerosis. However, the role of telomeres in CXCL12-mediated senescence-induced atherosclerosis remains obscure. This study aimed to unravel the role of CXCL12 and its association with telomeres in the context of menopause-induced arterial senescence and atherosclerosis. Apoe–/– mice underwent bilateral ovariectomy (OVX) to simulate early and late postmenopausal (EPM) conditions (1 and 5 weeks post-OVX, respectively). POL5551, a selective CXCR4 antagonist, was administered as a continuous infusion (30 mg/kg/day in PBS) using a subcutaneously implanted osmotic minipump for two weeks. ATP binding cassette transporter A1 (ABCA1), a cholesterol efflux regulator was significantly downmodulated (p < 0.05), while NOD-, LRR- and pyrin domain-containing protein 3 (NLR) family pyrin domain containing 3 (NLRP3), inducible nitric oxide synthase (iNOS) and the inflammatory mediators were considerably enhanced (p < 0.05) in both EPM and LPM mice groups. Notably, atherosclerosis was more prominent in the EPM than in the LPM mice. However, POL5551 treatment effectively ameliorated the reduced ABCA1 expression and the increased inflammatory response. Hence, we propose that inhibition of CXCL12 proffers robust anti-senescent and anti-atherosclerotic effects.