本文選題：心肌缺血再灌注損傷 + 腺苷酸活化蛋白激酶��； 參考：《山東醫(yī)藥》2017年17期

【摘要】：腺苷酸活化蛋白激酶(AMPK)作為心肌細(xì)胞的能量感受器,其不僅能調(diào)節(jié)并感知心肌細(xì)胞內(nèi)的能量狀態(tài),還能在心肌細(xì)胞缺血、缺氧條件下被激活,通過抑制ATP的消耗代謝途徑,刺激ATP的生成代謝途徑,維持心肌細(xì)胞的能量穩(wěn)態(tài),減少能量供應(yīng)不足對(duì)心肌產(chǎn)生的損傷。此外,激活的AMPK還能通過抑制內(nèi)質(zhì)網(wǎng)應(yīng)激、抑制細(xì)胞凋亡、優(yōu)化能量代謝、調(diào)節(jié)自噬等作用減少缺血-再灌注過程中心肌細(xì)胞的損害面積,從而延長(zhǎng)心肌細(xì)胞的存活率。
[Abstract]:Adenylate activated protein kinase (AMPK), as an energy receptor of cardiomyocytes, not only regulates and perceives the energy state in cardiomyocytes, but also can be activated during myocardial ischemia and hypoxia by inhibiting the pathway of ATP consumption and metabolism. Stimulating the metabolic pathway of ATP, maintaining the energy homeostasis of myocardial cells and reducing the damage caused by insufficient energy supply. In addition, activated AMPK can inhibit endoplasmic reticulum stress, inhibit cell apoptosis, optimize energy metabolism, regulate autophagy and reduce the area of myocardial cell damage during ischemia-reperfusion, thus prolonging the survival rate of cardiomyocytes.
【作者單位】： 遵義醫(yī)學(xué)院附屬醫(yī)院;
【基金】：國(guó)家自然科學(xué)基金項(xiàng)目(81360035、81560058) 貴州省科技攻關(guān)重點(diǎn)項(xiàng)目(黔科合SZ字2014-3022號(hào)) 貴州省教育廳自然科學(xué)招標(biāo)項(xiàng)目(黔教科合KY字2013-165號(hào))
【分類號(hào)】：R54

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