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FGF1 as a New Promising Therapeutic Target in Type 2 Diabetes: Advances in Research and Clinical Trials  ( SCI-EXPANDED收录)  

文献类型:期刊文献

英文题名:FGF1 as a New Promising Therapeutic Target in Type 2 Diabetes: Advances in Research and Clinical Trials

作者:Bu, Tiansheng[1];Gao, Xiaojuan[1];Zhang, Ruina[1];Xu, Ying[1]

第一作者:Bu, Tiansheng

通信作者:Xu, Y[1]

机构:[1]Gansu Univ Chinese Med, Affiliated Hosp 3, Dept Tradit Chinese Med, Baiyin, Gansu, Peoples R China

第一机构:甘肃中医药大学

通信机构:[1]corresponding author), Gansu Univ Chinese Med, Affiliated Hosp 3, Dept Tradit Chinese Med, Baiyin, Gansu, Peoples R China.|[10735]甘肃中医药大学;

年份:2025

卷号:18

起止页码:1137

外文期刊名:DIABETES METABOLIC SYNDROME AND OBESITY

收录:;Scopus(收录号:2-s2.0-105003779999);WOS:【SCI-EXPANDED(收录号:WOS:001470947600001)】;

基金:This study was partially funded by an internal project of Baiyin City First People's Hospital (2022YK-14).

语种:英文

外文关键词:FGF1; T2DM; insulin sensitivity; f-cell protection

摘要:Type 2 diabetes mellitus (T2DM) represents a global health crisis, characterized by insulin resistance, f -cell dysfunction, and metabolic disturbances. Current treatments, such as insulin and metformin, often fail to address the dual challenges of f -cell preservation and insulin resistance, leading to suboptimal long-term outcomes. Fibroblast growth factor 1 (FGF1) has recently gained attention as a new promising therapeutic target due to its unique ability to regulate glucose homeostasis, enhance insulin sensitivity, and protect f -cells without inducing hypoglycemia. This review critically examines the mechanisms of FGF1 action, including its signaling pathways, interactions with metabolic regulators, and roles in key organs involved in glucose metabolism. Additionally, we summarize findings from preclinical and clinical studies and evaluate the challenges associated with its therapeutic application, including pharmacokinetic limitations, delivery strategies, and long-term safety concerns. By addressing these issues, FGF1 holds the potential to advance beyond symptom management to become a disease-modifying therapy for T2DM.

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