2015
DOI: 10.1016/j.bbrc.2015.01.032
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Adipocytokine, omentin inhibits doxorubicin-induced H9c2 cardiomyoblasts apoptosis through the inhibition of mitochondrial reactive oxygen species

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Cited by 39 publications
(27 citation statements)
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“…Omentin suppresses agonist-stimulated hypertrophic response of cultured cardiac myocytes via activation of AMPK. Omentin is also reported to prevent doxorubicin-inducible cardiomyocyte death in vitro via suppression of mitochondrial reactive oxygen species 83) . Thus, these observations suggest that omentin serves as a cardioprotective adipocytokine (Fig.…”
Section: Resultsmentioning
confidence: 99%
“…Omentin suppresses agonist-stimulated hypertrophic response of cultured cardiac myocytes via activation of AMPK. Omentin is also reported to prevent doxorubicin-inducible cardiomyocyte death in vitro via suppression of mitochondrial reactive oxygen species 83) . Thus, these observations suggest that omentin serves as a cardioprotective adipocytokine (Fig.…”
Section: Resultsmentioning
confidence: 99%
“…High levels of ROS are associated with metabolic diseases like diabetes [16,20,36], which may contribute to the loss of myoblast function, increase myoblast cell death [33] and further exacerbate muscle repair in aging. Fulle and colleagues [25] have demonstrated that a high percentage of the myogenic precursor cells from elderly muscles undergo apoptosis triggered by mitochondrial-associated caspase-9 and this appears to be closely linked to the high ROS levels that are found in aged muscles [20].…”
Section: Introductionmentioning
confidence: 99%
“…Decreased serum level of omentin-1 was reported in polycystic ovary syndrome [6] , diabetes [7] and coronary artery disease [8] . Moreover, omentin was reported to prevent apoptosis of cardiomyoblasts via inhibition of mitochondrial ROS production [9] .…”
Section: Introductionmentioning
confidence: 99%