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多功能線粒體Epac1控制心肌細(xì)胞死亡

發(fā)布時間:2018-04-01 11:25

  本文選題:Epac 切入點:心肌細(xì)胞 出處:《中華高血壓雜志》2017年01期


【摘要】:正雖然第二信使環(huán)磷酸腺苷(cyclic AMP,cAMP)在生理上對心臟是有益的,但當(dāng)其調(diào)控失常時在很大程度上促進(jìn)心臟疾病進(jìn)展。目前的證據(jù)表明,cAMP是在線粒體內(nèi)產(chǎn)生的。然而,線粒體cAMP信號通路及其在心臟病理生理中的作用尚未知。該研究探討在缺血/再灌注(ischemia/reperfusion,I/R)損傷情況下,由cAMP 1直接激活的線粒體交換蛋白(mitochondrial exchange protein directly activated by cAMP 1,MitEpac1)的作用。研究發(fā)現(xiàn),Epac1基因切除
[Abstract]:Although is the second messenger cyclic AMP (cyclic AMP, cAMP) of the heart is beneficial in physiology, but when the regulation of arrhythmia largely promote heart disease progression. Current evidence suggests that cAMP is produced in mitochondria. However, mitochondrial cAMP signaling pathway and its role in the pathophysiology of heart is still unknown. The study on ischemia / reperfusion injury (ischemia/reperfusion, I/R) cAMP 1 cases by direct activation of mitochondrial protein (mitochondrial exchange protein directly exchange activated by cAMP 1, MitEpac1). The study found that Epac1 gene excision

【分類號】:R54
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本文編號:1695376

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