ACOT11 Gene Knockout Aggravates Kidney Tissue Fibrosis in UUO Mice
10.13241/j.cnki.pmb.2025.09.001
- VernacularTitle:ACOT11基因敲除后促进UUO模型小鼠肾脏组织纤维化
- Author:
Bo-liang KE
1
;
Chu-jiang HE
;
Qi-lin TANG
;
Wei-ming MOU
;
Yan ZHUANG
;
Yi SHAO
Author Information
1. 上海理工大学健康科学与工程学院 上海 200093;上海交通大学医学院附属第一人民医院泌尿外科 上海 200080
- Publication Type:Journal Article
- Keywords:
ACOT11;
Renal fibrosis;
Unilateral ureteral obstruction;
TGF-β
- From:
Progress in Modern Biomedicine
2025;25(9):1441-1451
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To explore the role and possible mechanism of ACOT11 in renal fibrosis model mice.Methods:A mouse model of renal fibrosis was established by unilateral ureteral obstruction(UUO)(Sham group and UUO7 group),and the expression of ACOT11 in the kidneys of UUO induced fibrosis mouse models was detected by protein immunoblotting and real-time fluorescence quantitative PCR(qRT-PCR).Subsequently,immunohistochemistry,Masson staining,H&E staining,PAS staining,and other experimental methods were used to detect the expression levels of fibrosis biomarkers fibronectin,α-SMA,and COL-1 in the kidneys of control and experimental group mice.In addition,by constructing ACOT11 gene knockout model mice and using the gene knockout model mice to construct a renal fibrosis model,the expression levels of fibrosis biomarkers such as fibronectin,α-SMA,COL-1,as well as fibrosis mechanism pathway related indicators TGF-β and Smad2 in the kidneys of each group of mice were further detected.Results:The results of WB and qRT-PCR experiments showed that the expression of ACOT11 in the kidney tissue of UUO model mice was significantly reduced compared to the Sham group.After knocking out the ACOT11 gene,H&E staining,PAS staining,and Masson staining showed that pathological inflammatory reactions such as abnormal glomerular and tubular structures,inflammatory cell infiltration and interstitial fibrous tissue proliferation in mice were significantly aggravated compared to the control group,and the expression of fibrosis markers Fibronectin,α-SMA,and COL-1 was significantly higher than that of the control group.Conclusion:ACOT11 plays a protective role in mice with unilateral ureteral obstruction model.After ACOT11 gene knockout,the fibrosis biomarkers of the mouse kidney increases and the degree of fibrosis worsens.
