Organ-differential Roles of Akt/FoxOs Axis as a Key Metabolic Modulator during Aging

下调和上调 蛋白激酶B PI3K/AKT/mTOR通路 内分泌学 磷酸化 生物 细胞生物学 信号转导 基因 生物化学
作者
Dae Hyun Kim,EunJin Bang,Sugyeong Ha,Hee Jin Jung,Yeon Ja Choi,Byung Pal Yu,Hae Young Chung
出处
期刊:Aging and Disease [Buck Institute for Research on Aging]
卷期号:12 (7): 1713-1713 被引量:15
标识
DOI:10.14336/ad.2021.0225
摘要

FoxOs and their post-translational modification by phosphorylation, acetylation, and methylation can affect epigenetic modifications and promote the expression of downstream target genes.Therefore, they ultimately affect cellular and biological functions during aging or occurrence of age-related diseases including cancer, diabetes, and kidney diseases.As known for its key role in aging, FoxOs play various biological roles in the aging process by regulating reactive oxygen species, lipid accumulation, and inflammation.FoxOs regulated by PI3K/Akt pathway modulate the expression of various target genes encoding MnSOD, catalases, PPARγ, and IL-1β during aging, which are associated with age-related diseases.This review highlights the age-dependent differential regulatory mechanism of Akt/FoxOs axis in metabolic and non-metabolic organs.We demonstrated that age-dependent suppression of Akt increases the activity of FoxOs (Akt/FoxOs axis upregulation) in metabolic organs such as liver and muscle.This Akt/FoxOs axis could be modulated and reversed by antiaging paradigm calorie restriction (CR).In contrast, hyperinsulinemia-mediated PI3K/Akt activation inhibited FoxOs activity (Akt/FoxOs axis downregulation) leading to decrease of antioxidant genes expression in non-metabolic organs such as kidneys and lungs during aging.These phenomena are reversed by CR.The results of studies on the process of aging and CR indicate that the Akt/FoxOs axis plays a critical role in regulating metabolic homeostasis, redox stress, and inflammation in various organs during aging process.The benefical actions of CR on the Akt/FoxOs axis in metabolic and non-metabolic organs provide further insights into the molecular mechanisms of organ-differential roles of Akt/FoxOs axis during aging.

科研通智能强力驱动
Strongly Powered by AbleSci AI
科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
1秒前
安德鲁完成签到,获得积分10
1秒前
JLUO发布了新的文献求助10
1秒前
玩命的囧发布了新的文献求助10
1秒前
江帆完成签到,获得积分20
2秒前
pbhhhhh发布了新的文献求助10
2秒前
HJJHJH发布了新的文献求助10
2秒前
蔺白发布了新的文献求助10
2秒前
目眩发布了新的文献求助30
3秒前
Jobs完成签到,获得积分10
4秒前
温暖白昼完成签到,获得积分10
4秒前
冬青完成签到,获得积分10
4秒前
活泼的向日葵完成签到,获得积分10
5秒前
JamesPei应助zzz1采纳,获得10
6秒前
你好发布了新的文献求助10
6秒前
JLUO完成签到,获得积分10
7秒前
7秒前
7秒前
年轻的星月完成签到,获得积分10
8秒前
脑洞疼应助吱吱吱吱采纳,获得10
8秒前
HJJHJH完成签到,获得积分10
9秒前
cxqygdn完成签到,获得积分10
9秒前
直率不乐完成签到,获得积分10
10秒前
Akim应助Jasen采纳,获得10
11秒前
GRQ发布了新的文献求助10
11秒前
地球发布了新的文献求助10
12秒前
12秒前
无花果应助直率不乐采纳,获得10
12秒前
12秒前
派大星发布了新的文献求助10
13秒前
踏实的青易完成签到 ,获得积分10
13秒前
科研通AI6.2应助我爱科研采纳,获得30
14秒前
cdercder应助史迪仔采纳,获得10
15秒前
向南完成签到,获得积分10
16秒前
llllll发布了新的文献求助10
16秒前
迷路路人完成签到,获得积分10
16秒前
522完成签到,获得积分10
17秒前
17秒前
Huan完成签到 ,获得积分10
18秒前
共享精神应助清许采纳,获得10
18秒前
高分求助中
(应助此贴封号)【重要!!请各用户(尤其是新用户)详细阅读】【科研通的精品贴汇总】 10000
Cronologia da história de Macau 5000
Braunwald’s Heart Disease, 2 Vol Set A Textbook of Cardiovascular Medicine 13th Edition 1000
Petrology and Plate Tectonics 800
Prompt Engineering for Clinicians: Harnessing AI in Everyday Medical Practice 600
Electrode Potentials 550
Handbook Of Synthetic Methodologies And Protocols Of Nanomaterials 500
热门求助领域 (近24小时)
化学 材料科学 医学 生物 纳米技术 工程类 有机化学 化学工程 生物化学 计算机科学 内科学 物理 复合材料 催化作用 细胞生物学 光电子学 物理化学 电极 基因 免疫学
热门帖子
关注 科研通微信公众号,转发送积分 6994376
求助须知:如何正确求助?哪些是违规求助? 8670309
关于积分的说明 18383251
捐赠科研通 6466580
什么是DOI,文献DOI怎么找? 3097965
关于科研通互助平台的介绍 2160372
邀请新用户注册赠送积分活动 2074479