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ELIMINATION OR NEUTRALIZATION OF ENDOGENOUS HIGH MOLECULAR WEIGHT FGF-2 INCREASES CARDIAC RESISTANCE TO DOXORUBICIN-INDUCED DAMAGE
ELIMINATION OR NEUTRALIZATION OF ENDOGENOUS HIGH MOLECULAR WEIGHT FGF-2 INCREASES CARDIAC RESISTANCE TO DOXORUBICIN-INDUCED DAMAGE
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机译:消除或中和内源性高分子量FGF-2会增加对阿霉素引起的损伤的抗药性
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摘要
Doxorubicin (Dox), a potent anti-cancer drug, can cause cardiac dysfunction and failure. Endogenous Fibroblast Growth Factor-2 (FGF2), a protein implicated in cardioprotection, regulates cardiac vulnerability to Dox. In wild type mice and in humans, cardiac FGF2 is composed of a mixture of mostly high (Hi-) but also low (Lo) molecular weight isoforms and is produced mainly by non- myocytes. We compared wild type mice, FGF2(WT), to mice genetically engineered as to express: no FGF2, FGF2(-); only Hi-FGF2, FGF2(Hi); only Lo- FGF2, FGF2(Lo). Sole expression of endogenous L0-FGF2 in vivo, or by fibroblasts in vitro, protects cardiomyocytes from Dox. In a wild type environment, neutralization of endogenous Hi-FGF2 presents a potential prophylactic treatment against Dox-induced cardiotoxicity.
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