期刊
JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
卷 19, 期 3, 页码 595-607出版社
WILEY
DOI: 10.1111/jcmm.12346
关键词
bFGF; endoplasmic reticulum stress; mitochondrial dysfunction; myocardial ischaemia; reperfusion
资金
- National Natural Science Foundation of China [81170203, 81302775]
- Zhejiang Provincial Program for the Cultivation of High-level Innovative Health talents
- State Key Basic Research Development Program [2012CB518105]
- Zhejiang Provincial Project of Protein Medicine Key Group [2010R50042]
Extensive research focused on finding effective strategies to prevent or improve recovery from myocardial ischaemia/reperfusion (I/R) injury. Basic fibroblast growth factor (bFGF) has been shown to have therapeutic potential in some heart disorders, including ischaemic injury. In this study, we demonstrate that bFGF administration can inhibit the endoplasmic reticulum (ER) stress and mitochondrial dysfunction induced in the heart in a mouse model of I/R injury. In vitro, bFGF exerts a protective effect by inhibiting the ER stress response and mitochondrial dysfunction proteins that are induced by tert-Butyl hydroperoxide (TBHP) treatment. Both of these in vivo and in vitro effects are related to the activation of two downstream signalling pathways, PI3K/Akt and ERK1/2. Inhibition of these PI3K/Akt and ERK1/2 pathways by specific inhibitors, LY294002 and PD98059, partially reduces the protective effect of bFGF. Taken together, our results indicate that the cardioprotective role of bFGF involves the suppression of ER stress and mitochondrial dysfunction in ischaemic oxidative damage models and oxidative stress-induced H9C2 cell injury; furthermore, these effects underlie the activation of the PI3K/Akt and ERK1/2 signalling pathways.
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