脂肪因子
调解人
不育
医学
信号转导
女性不育
生物信息学
失调家庭
内分泌学
内科学
肥胖
激素
生物
磷酸肌醇3激酶
瘦素
脂质信号
蛋白激酶A
卵泡期
糖尿病
机制(生物学)
胰岛素
雌激素
炎症
PI3K/AKT/mTOR通路
胰岛素抵抗
脂肪组织
代谢紊乱
细胞信号
胰岛素受体
小RNA
生殖系统
通路分析
作者
Gunvanti Rathod,Pragnesh Parmar
出处
期刊:Current Protein & Peptide Science
[Bentham Science Publishers]
日期:2026-03-30
卷期号:27
标识
DOI:10.2174/0113892037468611260302083920
摘要
Obesity-related female infertility is a result of the intricate interplay between metabolic disorders and reproductive abnormalities. The Phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) signaling pathway is an important molecular mediator that translates insulin action, adipokine function, and ovarian physiology. In obesity, the aberrant regulation of protein and peptide mediators of this pathway, such as insulin, adipokines, gonadotropins, and inflammatory cytokines, results in dysfunctional follicular growth, hormonal dysregulation, and decreased endometrial receptibility. Recent studies indicate that modulation of the PI3K/AKT pathway may provide novel therapeutic strategies to manage both metabolic and reproductive complications of obesity. This article focuses on the mechanistic and clinical implications of PI3K/AKT pathway dysfunction in obesity-related female infertility.
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