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甘丙肽通过 FoxO1 通路促进肥大心脏中的自噬并减轻细胞凋亡。

Galanin promotes autophagy and alleviates apoptosis in the hypertrophied heart through FoxO1 pathway.

机构信息

National Institute of Health and Medical Research (INSERM) U1048, 31432, Toulouse, Cedex 4, France; Paul Sabatier University, 31062, Toulouse, Cedex 9, France.

Paul Sabatier University, 31062, Toulouse, Cedex 9, France; Centre de Recherches en Cancérologie de Toulouse (CRCT), 2 Avenue Hubert Curien, 31037, Toulouse, France.

出版信息

Redox Biol. 2021 Apr;40:101866. doi: 10.1016/j.redox.2021.101866. Epub 2021 Jan 16.

Abstract

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.

摘要

自噬和细胞凋亡是细胞代谢和稳态多方面的强大调节剂。在这里,我们发现甘丙肽是一种多功能肽,通过叉头框蛋白 O1(FoxO1)通路调节心脏自噬并使凋亡性细胞死亡失活。在肥大的心脏中,甘丙肽促进自噬和代谢从脂肪酸(FA)向葡萄糖氧化转变,并维持线粒体完整性。在心肌细胞中,甘丙肽触发自噬体形成并减轻肥大、凋亡性细胞死亡和线粒体应激。在机制上,甘丙肽通过 FoxO1 通路决定细胞自噬和抗凋亡表型。总之,这些发现揭示了甘丙肽在调节心脏自噬中的一个以前未知的作用,并为支持心脏肥大重编程中细胞存活的分子机制提供了新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d1d0/7823211/96fabb2644a4/gr4.jpg

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