Cell Death Dis:PHB2缺乏会损害心脏脂肪酸氧化反应并导致心力衰竭

2020-03-23 QQY MedSci原创

心力衰竭作为一种复杂的临床综合征,是现代社会发病率及死亡率的主要原因之一。心力衰竭的发病机制涉及多种机制,包括代谢紊乱、线粒体功能障碍、细胞自噬、细胞凋亡以及遗传或表观遗传的失调。心力衰竭潜在机制的研

心力衰竭作为一种复杂的临床综合征,是现代社会发病率及死亡率的主要原因之一。心力衰竭的发病机制涉及多种机制,包括代谢紊乱、线粒体功能障碍、细胞自噬、细胞凋亡以及遗传或表观遗传的失调。心力衰竭潜在机制的研究对于其治疗至关重要。

脂肪酸是成人心脏能量产生的最主要的底物来源。PHB2(抑制素2)是一种位于线粒体内膜上的高度保守的蛋白质,其在细胞能量代谢稳态中起着关键的作用。但是其在调节心脏脂肪酸代谢中的功能仍然未知。

该研究发现心脏特异性敲除Phb2会导致脂肪滴积累导致心力衰竭。机制研究发现,PHB2缺失会通过下调CPT1b(肉碱棕榈酰转移酶1b,一种心脏线粒体脂肪酸氧化限速酶)来损害心脏脂肪酸氧化(FAO)反应。此外,过表达CPT1b能够减轻PHB2缺失的心肌细胞中受损的FAO反应。以上结果为PHB2与心脏脂肪酸代谢之间的关系提供了直接的证据。

综上,该研究发现PHB2是心脏线粒体内膜中潜在的脂肪酸氧化反应的调节因子,同时也证实了PHB2与CPT1b的关系以及其对心脏病理尤其是心脏脂肪酸代谢紊乱的影响。

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    2020-05-12 docwu2019
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    2020-03-25 cy0328

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