2001
DOI: 10.1172/jci200111334
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Inhibition of cyclooxygenase-2 aggravates doxorubicin-mediated cardiac injury in vivo

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Cited by 164 publications
(67 citation statements)
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References 31 publications
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“…Both COX-2 and its PGI 2 and PGE 2 products have been implicated in cardioprotection: prevention against oxidative injury via activation of the IP or the EP3 (21, 33) and ischemic preconditioning via COX-2 (22). Here, as previously observed in other species (21,22), the dominant prostaglandin (PG) formed by the heart is PGI 2 , and the second most abundant PG is PGF 2␣ (Fig. S2).…”
Section: Discussionsupporting
confidence: 63%
See 1 more Smart Citation
“…Both COX-2 and its PGI 2 and PGE 2 products have been implicated in cardioprotection: prevention against oxidative injury via activation of the IP or the EP3 (21, 33) and ischemic preconditioning via COX-2 (22). Here, as previously observed in other species (21,22), the dominant prostaglandin (PG) formed by the heart is PGI 2 , and the second most abundant PG is PGF 2␣ (Fig. S2).…”
Section: Discussionsupporting
confidence: 63%
“…One such example was an overview-trial analysis interpreted to suggest that arrhythmia, cardiac arrest, and sudden cardiac death might result from off target effects of rofecoxib (18). However, the dominant products of cardiomyocyte (CM) COX-2 are PGI 2 and PGE 2 , and deletion of the IP exacerbates ischemia reperfusion injury in mice (19) and inhibition of COX-2 exacerbates doxorubicininduced cardiotoxicity in vitro (20) and in vivo (21), an effect attenuated by PGI 2 analogues. COX-2-derived PGI 2 and PGE 2 have both been implicated as mediators of cardioprotection in late-phase ischemic preconditioning (22,23).…”
mentioning
confidence: 99%
“…Among doxorubicin alone treated group, the significant increase in LDH levels were revealed in all tested periods of time only at highest dose of this drug. These results are consistent with the previously reported results which had shown an elevation in LDH activity in rats receiving single and repeated doses of doxorubicin [2,9,10]. Significant increase in total LDH activity and cardiac isoform activity was also described by Al-Shabanah et al [3] even at 3 h after treatment with 15 mg doxorubicin/kg, what implies that source of the enzyme can be cardiomyocytes.…”
Section: Discussionsupporting
confidence: 92%
“…However, chronic inhibition of COX2 results in undesirable cardiovascular and gastrointestinal side effects that are due, in part, to reduced levels of prostacyclin PGI 2 and thromboxane A 2 (30,31). Thus, based on the obtained results, it is reasonable to suggest that selective targeting PGE 2 -forming enzyme mPGES1 or targeted genetic overexpression of PGE 2 -degrading enzyme 15-PGDH could provide more effective and safe way to combat cancer.…”
Section: Resultsmentioning
confidence: 97%