2019
DOI: 10.1038/s41591-019-0633-x
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Exercise reduces inflammatory cell production and cardiovascular inflammation via instruction of hematopoietic progenitor cells

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Cited by 192 publications
(191 citation statements)
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References 78 publications
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“…Increased marrow adipocytes, in turn, reduce the number of HSCs [70−72]. In contrast, a recent study suggests that exercise reduces leptin, a hormone that governs energy expenditure, and reduction of leptin instructs BMSCs to express HSC niche factors to promote HSC quiescence [73]. These studies illuminate the links between metabolic and physical conditions to the bone marrow microenvironment to support HSCs, with obesity and exercise negatively and positively affecting HSCs, respectively.…”
Section: Diet Metabolism and Clonal Hematopoiesismentioning
confidence: 99%
“…Increased marrow adipocytes, in turn, reduce the number of HSCs [70−72]. In contrast, a recent study suggests that exercise reduces leptin, a hormone that governs energy expenditure, and reduction of leptin instructs BMSCs to express HSC niche factors to promote HSC quiescence [73]. These studies illuminate the links between metabolic and physical conditions to the bone marrow microenvironment to support HSCs, with obesity and exercise negatively and positively affecting HSCs, respectively.…”
Section: Diet Metabolism and Clonal Hematopoiesismentioning
confidence: 99%
“…At high concentrations, leptin stimulates oxidative stress, inflammation, thrombosis, angiogenesis, and atherogenesis, which predispose CVD [109]. In contrast, voluntary physical activity reduces leptin signaling to the stromal hematopoietic bone marrow niche, consequently decreasing chronic hematopoietic output of inflammatory leukocytes and protecting from CVD [110].…”
Section: Leptinmentioning
confidence: 99%
“…Recently, Frodermann et al provided evidence that the exercise decreased the release of hematopoietic progenitor cells from the bone marrow by modulating the leptin release from the adipocyte. In this manner, the cardiovascular damage was relieved by lessening the inflammatory process [87]. This evidence gave us clues that the pathologic status induced the inflammatory differentiation of hematopoietic progenitor cells, and that such inflammation worsened the endothelial injury.…”
Section: Hematopoietic Progenitor Cells and Arterial Calcificationmentioning
confidence: 88%