2006
DOI: 10.1152/ajpheart.00395.2006
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Heat shock protects cardiac cells from doxorubicin-induced toxicity by activating p38 MAPK and phosphorylation of small heat shock protein 27

Abstract: . Heat shock protects cardiac cells from doxorubicin-induced toxicity by activating p38 MAPK and phosphorylation of small heat shock protein 27. Am J Physiol Heart Circ Physiol 291: H2680 -H2691, 2006. First published June 16, 2006 doi:10.1152/ajpheart.00395.2006 and its derivatives are used as chemotherapeutic drugs to treat cancer patients. However, production of DOX-mediated reactive oxygen species (ROS) by prolonged use of these drugs has been found to cause dilative cardiomyopathy and congestive heart fa… Show more

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Cited by 80 publications
(72 citation statements)
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References 47 publications
(64 reference statements)
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“…Recent evidence indicates that insulin activates ERK1/2 and p38 MAPK (3,25,35,41). p38 MAPK, in turn, activates MAPKAPK-2 that directly regulates the phosphorylation of Hsp27 (1,39,69). Ser15 and Ser85 phosphorylation of Hsp27 by MAPKAPK-2 is the key mechanism in reduction of apoptosis and facilitation of F-actin remodeling that protects cells from doxorubicin toxicity (69).…”
Section: Discussionmentioning
confidence: 99%
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“…Recent evidence indicates that insulin activates ERK1/2 and p38 MAPK (3,25,35,41). p38 MAPK, in turn, activates MAPKAPK-2 that directly regulates the phosphorylation of Hsp27 (1,39,69). Ser15 and Ser85 phosphorylation of Hsp27 by MAPKAPK-2 is the key mechanism in reduction of apoptosis and facilitation of F-actin remodeling that protects cells from doxorubicin toxicity (69).…”
Section: Discussionmentioning
confidence: 99%
“…p38 MAPK, in turn, activates MAPKAPK-2 that directly regulates the phosphorylation of Hsp27 (1,39,69). Ser15 and Ser85 phosphorylation of Hsp27 by MAPKAPK-2 is the key mechanism in reduction of apoptosis and facilitation of F-actin remodeling that protects cells from doxorubicin toxicity (69). Further evidence for phosphorylation of Hsp27 having a role in myocardial protection is provided by studies on activation of the p44/42 MAPK (ERK1/2) and p38 MAPK pathways by atorvastatin (20) and on activation of the adenosine A 1 receptor and p38 MAPK (14).…”
Section: Discussionmentioning
confidence: 99%
“…The expression and/or phosphorylation of hsp27 in the heart is increased in response to chronic pressure overload [20], both physiological and pathological hypertrophy [13], heart failure [21,38,39], oxidative stress [24,25], ischemic injury [22], and haemorrhagic shock [23]. Increased hsp27 expression prevents cardiac dysfunction and hypertrophy during chronic pressure overload [13], protects against doxorubicin-induced cardiomyopathy [26,27], and prevents tachypacing-induced atrial remodelling and atrial fibrillation [14,17,16,19]. The ability of heat shock to protect against doxorubicin-induced cardiomyopathy involves an increase in p38 activity and hsp27 phosphorylation [26,27].…”
Section: Discussionmentioning
confidence: 99%
“…Increased hsp27 expression prevents cardiac dysfunction and hypertrophy during chronic pressure overload [13], protects against doxorubicin-induced cardiomyopathy [26,27], and prevents tachypacing-induced atrial remodelling and atrial fibrillation [14,17,16,19]. The ability of heat shock to protect against doxorubicin-induced cardiomyopathy involves an increase in p38 activity and hsp27 phosphorylation [26,27]. Furthermore, the protective effects of hsp27 in tachypacing were prevented by a phosphodefective mutant of hsp27 [16].…”
Section: Discussionmentioning
confidence: 99%
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