2012
DOI: 10.1271/bbb.120423
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The PPARγ Agonist Protects Cardiomyocytes from Oxidative Stress and ApoptosisviaThioredoxin Overexpression

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Cited by 18 publications
(14 citation statements)
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“…In another study, Abaraviciene et al have also reported that RSG counteracts palmitate‐induced β ‐cell dysfunction by suppression of MAP kinase, inducible nitric oxide synthase and caspase‐3 activities . The protective role of RSG against apoptosis has also been reported in the other cells such as liver, endothelial, cardiomyocytes and sebocytes . In contrast to these findings, it has been reported that RSG may promote apoptosis.…”
Section: Discussionmentioning
confidence: 96%
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“…In another study, Abaraviciene et al have also reported that RSG counteracts palmitate‐induced β ‐cell dysfunction by suppression of MAP kinase, inducible nitric oxide synthase and caspase‐3 activities . The protective role of RSG against apoptosis has also been reported in the other cells such as liver, endothelial, cardiomyocytes and sebocytes . In contrast to these findings, it has been reported that RSG may promote apoptosis.…”
Section: Discussionmentioning
confidence: 96%
“…Treatment with RSG increases apoptosis of the cancer cells . In contrast, it was reported that RSG protects cardiomyocytes from H 2 O 2 ‐induced apoptosis . There are also data indicating that TZDs have preservative effects on the function and mass of the beta cells .…”
Section: Introductionmentioning
confidence: 97%
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“…The rosiglitazone-induced reduction in calcification was inhibited by a PPAR-gamma antagonist, confirming the salutary effect of activation of the PPAR-gamma agonist pathway (14). Kim and coworkers (15) suggested that rosiglitazone has a protective effect on oxidatively stressed cardiomyocytes via the thioredoxin system. H 2 O 2 -induced apoptosis was prevented by rosiglitazone via thioredoxin overexpression and other PPAR-gamma-dependent mechanisms, such as increased superoxide dismutase, pAkt/Akt, pERK/ERK, survivin, Bcl-2/Bax-α, and decreased caspase-3 and p53 (15).…”
Section: Discussionmentioning
confidence: 99%
“…PPARc activation is also shown to upregulate thioredoxin, survivin, and Bcl-2 leading to cardiac myocyte protection through inhibition of apoptosis [130]. Furthermore, hypercholesterolemic animals treated with rosiglitazone show reduced ischemic heart injury through reduced postischemic caspase-3 activation [131].…”
Section: Ppars In the Regulation Of Cardiac Cell Deathmentioning
confidence: 99%