TBC1D25 alleviates nonalcoholic steatohepatitis by inhibiting abnormal lipid accumulation and inflammation

被引：2

作者：

Wu, Anding ^{[1
]}

Ye, Mao ^{[2
]}

Ma, Tengfei ^{[3
]}

She, Zhigang ^{[4
]}

Li, Ruyan ^{[4
]}

Shi, Hongjie ^{[5
]}

Yang, Ling ^{[5
]}

Yi, Maolin ^{[6
]}

Li, Huoping ^{[2
]}

机构：

[1] Huanggang Cent Hosp, Dept Gen Surg, Huanggang, Peoples R China

[2] HuangGang Cent Hosp, Dept Cardiol, Huanggang, Peoples R China

[3] Huanggang Cent Hosp, Dept Neurol, Huanggang, Peoples R China

[4] Renmin Hosp Wuhan Univ, Dept Cardiol, Wuhan, Peoples R China

[5] Huanggang Inst Translat Med, Huanggang, Peoples R China

[6] Huanggang Cent Hosp, Surg Mammary Gland & Thyroid Gland, Huanggang, Peoples R China

来源：

JOURNAL OF CELLULAR PHYSIOLOGY | 2023年 / 238卷 / 02期

关键词：

fibrosis; hepatic steatosis; inflammation; NASH; TAK1; FATTY LIVER-DISEASE; ACTIVATION; MODELS;

D O I：

10.1002/jcp.30934

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Nonalcoholic fatty liver disease (NAFLD) is a strong stimulant of cardiovascular diseases, affecting one-quarter of the world's population. TBC1 domain family member 25 (TBC1D25) regulates the development of myocardial hypertrophy and cerebral ischemia-reperfusion injury; however, its effect on NAFLD/nonalcoholic steatohepatitis (NASH) has not been reported. In this study, we demonstrated that TBC1D25 expression is upregulated in NASH. TBC1D25 deficiency aggravated hepatic steatosis, inflammation, and fibrosis in NASH. In vitro tests revealed that TBC1D25 overexpression restrained NASH responses. Subsequent mechanistic validation experiments demonstrated that TBC1D25 interfered with NASH progression by inhibiting abnormal lipid accumulation and inflammation. TBC1D25 deficiency significantly promoted NASH occurrence and development. Therefore, TBC1D25 may potentially be used as a clinical therapeutic target for NASH treatment.

引用

页码：393 / 406

页数：14

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