Hyperglycemia-driven VEGF-A production is mediated by elevated O-GlcNAc modification of the Sp1 transcription factor. This mechanism may be significant in the pathogenesis of preclinical DR through VEGF-A upregulation.

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BackgroundGalectin-3 and soluble suppression of tumorigenicity-2 (sST2) are promising biomarkers of cardiac fibrosis and ventricular remodeling. The purpose of this study was to investigate the diagnostic and predictive value of galectin-3 and sST2 for use in patients who have heart failure with preserved ejection fraction (HFpEF).Material/MethodsA total of 217 hospitalized patients with HF and 30 controls from a physical examination center were included. Venous blood was collected for the detection of circulating expression of galectin-3 and sST2. All the included patients were followed up regularly for 1 year (12±1 months).ResultsThe concentrations of galectin-3 and NT-proBNP were substantially higher following decreased ejection fraction (both P=0.000), except for sST2 (P=0.068 vs. control). In ROC analyses, galectin-3 and NT-proBNP distinguished HFpEF from controls with an area under the curve (AUC) of 0.819 (95% CI: 0.75–0.89, P=0.000) and 0.806 (95% CI: 0.66–0.82, P=0.000). In contrast, sST2 obtained a lower AUC of 0.584 (95% CI: 0.49–0.68, P=0.17) compared to galectni-3 and NT-proBNP. After adjustment for clinical factors and NT-proBNP, galectin-3 was strongly correlated with an increased risk of the endpoint events in HFpEF patients, and the hazard ratio per 1 SD increase of the galectin-3 level was 2.33 (95%CI: 1.72–2.94, P=0.009).ConclusionsGalectin-3 is superior to sST2 in distinguishing HFpEF from controls and HFrEF.

During myocardial infarction, quickly opening the occluded coronary artery is a major method to save the ischemic myocardium. However, it also induces reperfusion injury, resulting in a poor prognosis. Alleviating the reperfusion injury improves the prognosis of the patients. Dihydromyricetin (DHM), a major component in the Ampelopsis grossedentata, has numerous biological functions. This study aims to clarify the effects of DHM under the ischemia/reperfusion (I/R) condition. We elucidated the role of Sirt3 in the cardiomyocyte response to DHM based on the hearts and primary cardiomyocytes. Cardiac function, mitochondrial biogenesis, and infarct areas were examined in the different groups. We performed Western blotting to detect protein expression levels after treatments. In an in vitro study, primary cardiomyocytes were treated with Hypoxia/Reoxygenation (H/R) to simulate the I/R. DHM reduced the infarct area and improved cardiac function. Furthermore, mitochondrial dysfunction was alleviated after DHM treatment. Moreover, DHM alleviated oxidative stress indicated by decreased ROS and MnSOD. However, the beneficial function of DHM was abolished after removing the Sirt3. On the other hand, the mitochondrial function was improved after DHM intervention in vitro study. Interestingly, Sirt3 downregulation inhibited the beneficial function of DHM. Therefore, the advantages of DHM are involved in the improvement of mitochondrial function and decreased oxidative stress through the upregulation of Sirt3. DHM offers a promising therapeutic avenue for better outcome in the patients with cardiac I/R injury.