2020
DOI: 10.1007/s10741-020-09996-y
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Beyond the myocardium? SGLT2 inhibitors target peripheral components of reduced oxygen flux in the diabetic patient with heart failure with preserved ejection fraction

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Cited by 3 publications
(1 citation statement)
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“…The induction of TNF-α from sarcopenic obesity inhibits adiponectin while negatively impacting myocyte mitochondrial biogenesis and myogenesis, causing a vicious cycle within sarcopenia obesity of decreased muscle mass and increased adiposity [64]. Overexpression of TNF-α from sarcopenic obesity also downregulates eNOS, further exacerbating hemodynamics, while promoting a negative ionotropic cardiac state [65,66]. Moreover, there is evidence to show that it promotes pathologic vascular and valvular calcification [67,68].…”
Section: The Sarcopenic Obesity Phenotype and Testosteronementioning
confidence: 99%
“…The induction of TNF-α from sarcopenic obesity inhibits adiponectin while negatively impacting myocyte mitochondrial biogenesis and myogenesis, causing a vicious cycle within sarcopenia obesity of decreased muscle mass and increased adiposity [64]. Overexpression of TNF-α from sarcopenic obesity also downregulates eNOS, further exacerbating hemodynamics, while promoting a negative ionotropic cardiac state [65,66]. Moreover, there is evidence to show that it promotes pathologic vascular and valvular calcification [67,68].…”
Section: The Sarcopenic Obesity Phenotype and Testosteronementioning
confidence: 99%