SAA3 deficiency exacerbates intestinal fibrosis in DSS-induced IBD mouse model.

Jan 27, 2025

Experts: Xiaodong Zou,Tong Wu,Jianjiao Lin,Tao Su,Hui Xiao,Chuyan Ni,Lijuan Hu,Wenchu Lin,Weilin Chen,Richard D Ye,Li Xiang

Intestinal fibrosis, as a late-stage complication of inflammatory bowel disease (IBD), leads to bowel obstruction and requires surgical intervention, significantly lowering the quality of life of affected patients. SAA3, a highly conserved member of the serum amyloid A (SAA) apolipoprotein family in mice, is synthesized primarily as an acute phase reactant in response to infection, inflammation and trauma. An increasing number of evidence suggests that SAA3 exerts a vital role in the fibrotic process, even though the underlying mechanisms are not yet fully comprehended. This study utilized dextran sulfate sodium (DSS) to establish an IBD mouse model and observed that the SAA3-deficient mice exhibited more severe intestinal fibrosis. Our results further indicated that SAA3 genetic disruption in fibroblasts enhanced cell activation to myofibroblasts through HSPB1/NF-κB/TGF-β1/Smads signaling cascade, exacerbating the pathological phenotype of intestinal fibrosis. Collectively, our results shed novel lights on regulating SAA3 in intestinal fibrosis and indicate the potential to develop therapeutic strategies for IBD patients.
© 2025. The Author(s).

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ABOUT THE EXPERTS

Xiaodong Zou,Tong Wu,Jianjiao Lin,Tao Su,Hui Xiao,Chuyan Ni,Lijuan Hu,Wenchu Lin,Weilin Chen,Richard D Ye,Li Xiang

Xiaodong Zou

Department of Gastroenterology, The Second Affiliated Hospital, School of Medicine, The Chinese University of Hong Kong, Shenzhen & Longgang District People’s Hospital of Shenzhen, Shenzhen, 518172, China.

Guangdong Key Laboratory for Biomedical Measurements and Ultrasound Imaging, National-Regional Key Technology Engineering Laboratory for Medical Ultrasound, School of Biomedical Engineering, Shenzhen University Medical School, Shenzhen, 518060, China.

Tong Wu

Kobilka Institute of Innovative Drug Discovery, School of Medicine, The Chinese University of Hong Kong, Shenzhen, Guangdong, China.

Jianjiao Lin

Department of Gastroenterology, The Second Affiliated Hospital, School of Medicine, The Chinese University of Hong Kong, Shenzhen & Longgang District People’s Hospital of Shenzhen, Shenzhen, 518172, China.

Tao Su

Department of Gastroenterology, The Second Affiliated Hospital, School of Medicine, The Chinese University of Hong Kong, Shenzhen & Longgang District People’s Hospital of Shenzhen, Shenzhen, 518172, China.

Hui Xiao

Department of Pathology, The Second Affiliated Hospital, School of Medicine, The Chinese University of Hong Kong, Shenzhen & Longgang District People’s Hospital of Shenzhen, Shenzhen, 518172, China.

Chuyan Ni

Department of Gastroenterology, The Second Affiliated Hospital, School of Medicine, The Chinese University of Hong Kong, Shenzhen & Longgang District People’s Hospital of Shenzhen, Shenzhen, 518172, China.

Lijuan Hu

Department of Gastroenterology, The Second Affiliated Hospital, School of Medicine, The Chinese University of Hong Kong, Shenzhen & Longgang District People’s Hospital of Shenzhen, Shenzhen, 518172, China.

Wenchu Lin

Institute of Digestive Disease, The Second Affiliated Hospital, School of Medicine, The Chinese University of Hong Kong, Shenzhen & Longgang District People’s Hospital of Shenzhen, Shenzhen, 518172, China.

Weilin Chen

Marshall Laboratory of Biomedical Engineering, Institute of Biological Therapy, Shenzhen University Medical School, Shenzhen University, Shenzhen, 518055, China.

Richard D Ye

Kobilka Institute of Innovative Drug Discovery, School of Medicine, The Chinese University of Hong Kong, Shenzhen, Guangdong, China. richardye@cuhk.edu.cn.

The Chinese University of Hong Kong, Shenzhen Futian Biomedical Innovation R&D Center, Shenzhen, China. richardye@cuhk.edu.cn.

Li Xiang

Department of Gastroenterology, The Second Affiliated Hospital, School of Medicine, The Chinese University of Hong Kong, Shenzhen & Longgang District People’s Hospital of Shenzhen, Shenzhen, 518172, China. shellyxiangli@163.com.