The pleiotropic association between IL-10 levels and CVD prognosis: Evidence from a meta-analysis

Ni, Shi-Hao; Sun, Shuning; Huang, Zeng-Yan; Huang, Yu‐Sheng; Li, Huan; Wang, Jiajia; Xian, Shaoxiang; Yang, Zhong-Qi; Wang, Lingjun; Lu, Lu

doi:10.1016/j.cyto.2019.02.017

Cited by 5 publications

(2 citation statements)

References 57 publications

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“…Snacking on almonds significantly decreased TC, LDL-C, and non-HDL-C by 5.5%, 4.6%, and 6.4% respectively, relative to the cookie control (p ≤ 0.05). Almonds also significantly reduced IL-10 compared to the cookie control by 22% (p < 0.04), and elevated levels have been associated with poor CVD prognosis [78]. There was a tendency to reduce inflammatory biomarkers intercellular adhesion molecule -1(ICAM-1), IL-1β, and IL-6 with almonds, compared to the cookies (p ≤ 0.187).…”

Section: Four To Six Weeks Durationmentioning

confidence: 92%

A Comprehensive Review of Almond Clinical Trials on Weight Measures, Metabolic Health Biomarkers and Outcomes, and the Gut Microbiota

Dreher

2021

Nutrients

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This comprehensive narrative review of 64 randomized controlled trials (RCTs) and 14 systematic reviews and/or meta-analyses provides an in-depth analysis of the effect of almonds on weight measures, metabolic health biomarkers and outcomes, and the colonic microbiota, with extensive use of figures and tables. Almonds are a higher energy-dense (ED) food that acts like a lower ED food when consumed. Recent systematic reviews and meta-analyses of nut RCTs showed that almonds were the only nut that had a small but significant decrease in both mean body mass and fat mass, compared to control diets. The biological mechanisms for almond weight control include enhanced displacement of other foods, decreased macronutrient bioavailability for a lower net metabolizable energy (ME), upregulation of acute signals for reduced hunger, and elevated satiety and increased resting energy expenditure. The intake of 42.5 g/day of almonds significantly lowered low-density lipoprotein cholesterol (LDL-C), 10-year Framingham estimated coronary heart disease (CHD) risk and associated cardiovascular disease (CVD) medical expenditures. Diastolic blood pressure (BP) was modestly but significantly lowered when almonds were consumed at >42.5 g/day or for >6 weeks. Recent RCTs suggest possible emerging health benefits for almonds such as enhanced cognitive performance, improved heart rate variability under mental stress, and reduced rate of facial skin aging from exposure to ultraviolet (UV) B radiation. Eight RCTs show that almonds can support colonic microbiota health by promoting microflora richness and diversity, increasing the ratio of symbiotic to pathogenic microflora, and concentrations of health-promoting colonic bioactives. Almonds are a premier healthy snack for precision nutrition diet plans.

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Section: Four To Six Weeks Durationmentioning

confidence: 92%

A Comprehensive Review of Almond Clinical Trials on Weight Measures, Metabolic Health Biomarkers and Outcomes, and the Gut Microbiota

Dreher

2021

Nutrients

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“…We observed that G-MDSCs increased the levels of proinflammatory cytokines, such as IL-6, IL-10, and TNF-α in fibroblasts. The aging process was shown to be associated with a balance between proinflammatory and anti-inflammatory responses, and MDSCs play an important role in this process 21,36,37 . A previous study indicated that activated MDSCs suppress the functions of invading inflammatory cells, limiting the excessive inflammatory response but promoting the presence of low-grade chronic inflammation 25 .…”

Section: Discussionmentioning

confidence: 99%

G-MDSCs promote aging-related cardiac fibrosis by activating myofibroblasts and preventing senescence

Sun

et al. 2021

Cell Death Dis

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Aging is one of the most prominent risk factors for heart failure. Myeloid-derived suppressor cells (MDSCs) accumulate in aged tissue and have been confirmed to be associated with various aging-related diseases. However, the role of MDSCs in the aging heart remains unknown. Through RNA-seq and biochemical approaches, we found that granulocytic MDSCs (G-MDSCs) accumulated significantly in the aging heart compared with monocytic MDSCs (M-MDSCs). Therefore, we explored the effects of G-MDSCs on the aging heart. We found that the adoptive transfer of G-MDSCs of aging mice to young hearts resulted in cardiac diastolic dysfunction by inducing cardiac fibrosis, similar to that in aging hearts. S100A8/A9 derived from G-MDSCs induced inflammatory phenotypes and increased the osteopontin (OPN) level in fibroblasts. The upregulation of fibroblast growth factor 2 (FGF2) expression in fibroblasts mediated by G-MDSCs promoted antisenescence and antiapoptotic phenotypes of fibroblasts. SOX9 is the downstream gene of FGF2 and is required for FGF2-mediated and G-MDSC-mediated profibrotic effects. Interestingly, both FGF2 levels and SOX9 levels were upregulated in fibroblasts but not in G-MDSCs and were independent of S100A8/9. Therefore, a novel FGF2-SOX9 signaling axis that regulates fibroblast self-renewal and antiapoptotic phenotypes was identified. Our study revealed the mechanism by which G-MDSCs promote cardiac fibrosis via the secretion of S100A8/A9 and the regulation of FGF2-SOX9 signaling in fibroblasts during aging.

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Arctigenin alleviates myocardial infarction injury through inhibition of the NFAT5-related inflammatory phenotype of cardiac macrophages/monocytes in mice

Sun

Zhou

et al. 2020

Laboratory Investigation

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The pleiotropic association between IL-10 levels and CVD prognosis: Evidence from a meta-analysis

Cited by 5 publications

References 57 publications

A Comprehensive Review of Almond Clinical Trials on Weight Measures, Metabolic Health Biomarkers and Outcomes, and the Gut Microbiota

A Comprehensive Review of Almond Clinical Trials on Weight Measures, Metabolic Health Biomarkers and Outcomes, and the Gut Microbiota

G-MDSCs promote aging-related cardiac fibrosis by activating myofibroblasts and preventing senescence

Arctigenin alleviates myocardial infarction injury through inhibition of the NFAT5-related inflammatory phenotype of cardiac macrophages/monocytes in mice

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