Age-associated declined function of endothelial progenitor cells and its correlation with plasma IL-18 or IL-23 concentrations in patients with ST-segment elevation myocardial infarction.

Background: ST-segment elevation myocardial infarction (STEMI) persists to be prevalent in the elderly with a dismal prognosis. The capacity of endothelial progenitor cells (EPCs) is reduced with aging. Nevertheless, the influence of aging on the functionality of EPCs in STEMI is not fully understood. Method: This study enrolled 20 younger STEMI patients and 21 older STEMI patients. We assessed the Thrombolysis in Myocardial Infarction (TIMI) and Global Registry of Acute Coronary Events Risk (GRACE) scores in two groups. Then, we detected EPC migration, proliferation, adhesion, and plasma interleukin (IL)-18 and IL-23 concentrations in two groups. In addition, we analyzed the interconnection between age, EPC function, plasma IL-18 and IL-23 concentrations, and GRACE or TIMI scores in STEMI patients. Result: GRACE and TIMI scores in older STEMI patients were higher than in younger STEMI patients, whereas EPC function declined. GRACE and TIMI scores were found to have an inverse relationship with the EPC function. In older STEMI patients, plasma concentrations of IL-18 and IL-23 increased. Plasma IL-18 and IL-23 concentrations were adversely connected to EPC capacity and positively related to GRACE and TIMI scores. Moreover, age was positively correlated with plasma IL-18 or IL-23 concentrations, as well as GRACE or TIMI scores. However, age was adversely correlated with EPC function. Conclusion: In patients with STEMI, aging results in declined EPC function, which may be associated with inflammatory cytokines. The current investigation may offer new perception about mechanism and therapeutic targets of aging STEMI.

Association Between Ultraprocessed Foods Consumption and Leucocyte Telomere Length: A Cross-Sectional Study of UK Biobank.

BACKGROUND: □ OBJECTIVES: This study aimed to investigate the association between consumption of ultraprocessed foods and leucocyte telomere length (LTL). METHODS: This cross-sectional study utilized data from the UK Biobank, including a total of 64,690 participants. LTL was measured using qPCR with natural logarithmic conversion and z-score normalization. Dietary data were collected through a 24-h recall questionnaire from 2009 to 2010. Ultraprocessed foods (UPFs) were identified using the NOVA food classification as either a continuous or a categorical variable. Multiple linear regression models were employed to analyze the association between UPF consumption and LTL. RESULTS: The included participants had an average age of 56.26 y, of whom 55.2% were female. After adjusting for demographic and health-related variables, LTL exhibited a decrease of 0.005 (95% CI: -0.007, -0.002) with 1 UPF serving increase. Compared with participants consuming ≤3.5 servings/d, those consuming 3.5 to <6 servings showed a shortening of LTL by 0.025 (95% CI: -0.046, -0.003). Participants consuming 6 to ≤8 servings/d and >8 servings/d had LTL shortening of 0.032 (95% CI: -0.054, -0.011) and 0.037 (95% CI: -0.060, -0.014), respectively (P for trend = 0.002). Subgroup analyses by UPF subclasses revealed that the consumption of ready-to-eat/heated food (ß: -0.010; 95% CI: -0.016, -0.004), beans and potatoes (ß: -0.027; 95% CI: -0.043, -0.012), animal-based products (ß: -0.012; 95% CI: -0.020, -0.005), artificial sugar (ß: -0.014; 95% CI:-0.025,-0.003), and beverages (ß: -0.005; 95% CI: -0.009, -0.001) showed negative associations with LTL. Conversely, breakfast cereals (ß: 0.022; 95% CI: 0.006, 0.038) and vegetarian alternatives (ß: 0.056; 95% CI:0.026,0.085) showed positive correlations with LTL. CONCLUSIONS: Our study found that a higher consumption of total UPF was associated with a shorter LTL. However, some UPFs may be associated with longer LTL, depending on their nutritional composition.

Aging-Related Endothelial Progenitor Cell Dysfunction and Its Association with IL-17 and IL-23 in HFmrEF Patients.

Background: Aging is an independent risk factor for heart failure (HF), and endothelial progenitor cell (EPC) function decreases with aging. Here, we further investigated whether age has a detrimental effect on circulating EPC function in HF with mildly reduced ejection fraction (HFmrEF) and its relationship with systemic inflammation. Methods: 58 HFmrEF patients were recruited. The adhesive, migrative, and proliferative activities of circulating EPCs, MAGGIC scores, and plasma interleukin (IL)-17 and IL-23 levels of these patients were assessed. Results: Older patients with HFmrEF had higher MAGGIC scores and lower circulating EPC adhesion, migration, and proliferation than younger patients. The similar tendency was observed in plasma IL-17 and IL-23 levels. The EPC functions were negatively associated with MAGGIC scores and plasma IL-17 or IL-23 levels. Conclusions: In patients with HFmrEF, aging leads to attenuated circulating EPC function, which is correlated with disease severity and systemic inflammation. The present investigation provides some novel insights into the mechanism and intervention targets of HFmrEF.

miR-340-5p Alleviates Oxidative Stress Injury by Targeting MyD88 in Sepsis-Induced Cardiomyopathy.

Background: Sepsis-induced cardiomyopathy (SIC) is a sort of severe disease in the intensive care unit. This research focuses on exploring the influence of miR-340-5p on SIC and its specific mechanism. Methods: Mice were administered with lipopolysaccharide (LPS) to construct a SIC animal model. Mice were intramyocardially injected with Adenoassociated Virus- (AAV-) 9 containing the miR-340-5p precursor to make the miR-340-5p overexpression in the myocardium. The expression level of myocardial miR-340-5p was evaluated by qRT-PCR. The cardiac function was measured by echocardiography, the myocardial morphology was observed by hematoxylin-eosin (HE) staining, and the oxidative stress level was detected by 4-hydroxynonenal (4-HNE) immunohistochemical staining and malondialdehyde (MDA) assay in mice. The cells were pretreated with miR-340-5p mimic, mimic-NC, miR-340-5p inhibitor, inhibitor-NC, MyD88 siRNA, or si-NC and then administered with LPS or PBS. The cell viability was measured with the CCK-8 assay. The level of intracellular oxidative stress was evaluated using reactive oxygen species (ROS), MDA, and glutathione (GSH) detection. The MyD88 level was assessed via Western blotting analysis. The interaction of miR-340-5p with the MyD88 mRNA was confirmed via dual-luciferase reporter assay and RNA pull-down assay. Results: The miR-340-5p overexpression partially alleviated the increase of the MyD88 level, impairment of cardiac function, and oxidative stress injury in the SIC animal model. In the SIC cell model, miR-340-5p mimic pretreatment partially relieved oxidative stress injury, while the miR-340-5p inhibitor had the opposite effect. Besides, the miR-340-5p mimic and inhibitor could reduce and further increase the MyD88 level in the SIC cell model, respectively. Dual-luciferase reporter and RNA pull-down experiments confirmed the interaction between the MyD88 mRNA and miR-340-5p. Finally, it was found that MyD88 siRNA pretreatment also partially alleviates the oxidative stress injury in the SIC cell model. Conclusion: In sum, our study demonstrated that miR-340-5p can improve myocardial oxidative stress injury by targeting MyD88 in SIC.