当前位置: X-MOL 学术Redox Biol. › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
Galanin promotes autophagy and alleviates apoptosis in the hypertrophied heart through FoxO1 pathway
Redox Biology ( IF 10.7 ) Pub Date : 2021-01-16 , DOI: 10.1016/j.redox.2021.101866
Ilenia Martinelli 1 , Andrei Timotin 1 , Paula Moreno-Corchado 1 , Dimitri Marsal 1 , Solomiia Kramar 1 , Halina Loy 1 , Carine Joffre 2 , Frederic Boal 1 , Helene Tronchere 1 , Oksana Kunduzova 1
Affiliation  

Autophagy and apoptosis are powerful regulators of multiple facets of cellular metabolism and homeostasis. Here, we uncover that galanin, a pleiotropic peptide, regulates cardiac autophagy and deactivates apoptotic cell death through the Forkhead box protein O1 (FoxO1) pathway. In hypertrophied heart, galanin promotes autophagy and metabolic shift from fatty acid (FA) to glucose oxidation and preserves mitochondrial integrity. In cardiomyoblasts, galanin triggers autophagosome formation and alleviates hypertrophy, apoptotic cell death, and mitochondrial stress. Mechanistically, galanin dictates cell autophagic and anti-apoptotic phenotypes through FoxO1 pathway. Together, these findings uncover a previously unknown role for galanin in the regulation of cardiac autophagy and provide new insights into the molecular mechanisms supporting cell survival in the hypertrophic reprogramming of the heart.



中文翻译:

甘丙肽通过FoxO1途径促进肥大心脏的自噬并减轻细胞凋亡

自噬和细胞凋亡是细胞代谢和体内稳态的多个方面的有力调节器。在这里,我们发现多效肽甘丙肽通过叉头盒蛋白O1(FoxO1)途径调节心脏自噬并失活凋亡性细胞死亡。在肥大的心脏中,甘丙肽促进自噬和代谢从脂肪酸(FA)转变为葡萄糖氧化,并保持线粒体完整性。在心肌母细胞中,甘丙肽触发自噬体形成并减轻肥大,凋亡细胞死亡和线粒体应激。从机制上讲,甘丙肽通过FoxO1途径决定细胞的自噬和抗凋亡表型。一起,

更新日期:2021-01-22
down
wechat
bug