PI3k/AKT信号通路在减轻肝纤维化中的作用:全面综述
Frontiers in Medicine
(
IF
3
)
Pub Date : 2024-03-25
, DOI:
10.3389/fmed.2024.1389329
Emad Shamsan
1,
2
,
Maged Almezgagi
1
,
Mohammed Gamah
1
,
Naveed Khan
1
,
Abdulkareem Qasem
2
,
Liu Chuanchuan
1,
3
,
Fan Haining
1,
3
Affiliation
College of Clinical Medicine, Qinghai University, Xining, China.
College of Medical Science, Taiz University, Taiz, Yemen.
Qinghai University Affiliated Hospital, Xining, China.
肝脏内细胞外基质(ECM)成分的过度积累会导致称为肝纤维化的病理状况。酗酒、非酒精性脂肪肝 (NAFLD)、自身免疫问题和病毒性肝炎会导致慢性肝损伤。探索潜在的治疗靶点并了解肝纤维化的分子机制对于制定有效的干预措施至关重要。这篇综合综述的目的是解释 PI3K/AKT 信号通路如何有助于减少肝纤维化。通过总结结果来研究该途径作为治疗靶点的潜力体内和体外研究。专注于 PI3K/AKT 激活的研究表明,纤维化标志物显着减少,肝功能显着改善。该综述强调了该途径如何阻止 ECM 合成和肝星状细胞 (HSC) 激活,最终减少纤维化反应。肝纤维化中 PI3K/AKT 通路的具体机制和下游效应器构成了一个快速发展的研究领域。总之,PI3K/AKT信号通路在减轻肝纤维化中发挥着重要作用。它在调节 HSC 激活和 ECM 产生中的复杂作用,证明了体外和体内,强调了其作为控制肝纤维化和减缓疾病进展的有效治疗方法的潜力。对该领域的全面回顾为其未来发展及其对临床应用的影响提供了宝贵的见解。
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The role of PI3k/AKT signaling pathway in attenuating liver fibrosis: a comprehensive review
Excessive accumulation of extracellular matrix (ECM) components within the liver leads to a pathological condition known as liver fibrosis. Alcohol abuse, non-alcoholic fatty liver disease (NAFLD), autoimmune issues, and viral hepatitis cause chronic liver injury. Exploring potential therapeutic targets and understanding the molecular mechanisms involved in liver fibrosis are essential for the development of effective interventions. The goal of this comprehensive review is to explain how the PI3K/AKT signaling pathway contributes to the reduction of liver fibrosis. The potential of this pathway as a therapeutic target is investigated through a summary of results from in vivo and in vitro studies. Studies focusing on PI3K/AKT activation have shown a significant decrease in fibrosis markers and a significant improvement in liver function. The review emphasizes how this pathway may prevent ECM synthesis and hepatic stellate cell (HSC) activation, ultimately reducing the fibrotic response. The specific mechanisms and downstream effectors of the PI3K/AKT pathway in liver fibrosis constitute a rapidly developing field of study. In conclusion, the PI3K/AKT signaling pathway plays a significant role in attenuating liver fibrosis. Its complex role in regulating HSC activation and ECM production, demonstrated both in vitro and in vivo, underscores its potential as a effective therapeutic approach for managing liver fibrosis and slowing disease progression. A comprehensive review of this field provides valuable insights into its future developments and implications for clinical applications.