Glucose-dependent insulinotropic polypeptide (GIP) alleviates ferroptosis in aging-induced brain damage through the Epac/Rap1 signaling pathway
  • Ko, Jiwon
  • Jang, Soyoung
  • Jang, Soyeon
  • Park, Song
  • Yi, Junkoo
  • 외 5명
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5
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5

초록

Glucose-dependent insulinotropic polypeptide (GIP), a 42-amino-acid hormone, exerts multifaceted effects in physiology, most notably in metabolism, obesity, and inflammation. Its significance extends to neuroprotection, promoting neuronal proliferation, maintaining physiological homeostasis, and inhibiting cell death, all of which play a crucial role in the context of neurodegenerative diseases. Through intricate signaling pathways involving its cognate receptor (GIPR), a member of the G protein-coupled receptors, GIP maintains cellular homeostasis and regulates a defense system against ferroptosis, an essential process in aging. Our study, utilizing GIP-overexpressing mice and in vitro cell model, elucidates the pivotal role of GIP in preserving neuronal integrity and combating age-related damage, primarily through the Epac/Rap1 pathway. These findings shed light on the potential of GIP as a therapeutic target for the pathogenesis of ferroptosis in neurodegenerative diseases and aging. © (2024), (The Biochemical Society of the Republic of Korea). All rights reserved.

키워드

AgingBrainEpac/Rap1FerroptosisGIP
제목
Glucose-dependent insulinotropic polypeptide (GIP) alleviates ferroptosis in aging-induced brain damage through the Epac/Rap1 signaling pathway
저자
Ko, JiwonJang, SoyoungJang, SoyeonPark, SongYi, JunkooChoi, Dong KyuKim, SeonggonKim, Myoung OkLim, Su-GeunRyoo, Zae Young
DOI
10.5483/BMBRep.2024-0067
발행일
2024-09
유형
Article
저널명
BMB Reports
57
9
페이지
417 ~ 423