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S100A9 promotes inflammatory response in diabetic nonalcoholic fatty liver disease.
- Source :
-
Biochemical & Biophysical Research Communications . Aug2022, Vol. 618, p127-132. 6p. - Publication Year :
- 2022
-
Abstract
- Nonalcoholic fatty liver disease (NAFLD) has been previously shown to be associated with diabetes mellitus (DM) which is one of the most decisive risk factors for the faster progression of NAFLD to nonalcoholic steatohepatitis (NASH), fibrosis or advanced cirrhosis. However, the critical molecular pathway involved in the development of diabetic-induced liver injury is unclear. By the proteomic study of liver from high-fat diet (HFD)/streptozotocin(STZ)-induced diabetic mice, we revealed that the upregulation of S100A9 was involved in the development of NAFLD with DM. Moreover, we found that S100A9 silencing decreased proinflammatory response and inhibited the TLR4-NF-κB signaling in in-vitro study. Our findings provide new perspectives into the pivotal role of S100A9 for development of diabetic NAFLD and revealed that S100A9 is a critical molecule that links liver injury to inflammation of NAFLD with DM. • Diabetes mellitus promoted the progression of NAFLD in HFD mice. • Upregulation of S100A9 was involved in the development of NAFLD with Diabetes. • S100A9 silencing decreased proinflammatory response and inhibited the TLR4-NF-κB signaling in HG-treated HepG2 cells. [ABSTRACT FROM AUTHOR]
- Subjects :
- *NON-alcoholic fatty liver disease
*INFLAMMATION
*HIGH-fat diet
Subjects
Details
- Language :
- English
- ISSN :
- 0006291X
- Volume :
- 618
- Database :
- Academic Search Index
- Journal :
- Biochemical & Biophysical Research Communications
- Publication Type :
- Academic Journal
- Accession number :
- 157711537
- Full Text :
- https://doi.org/10.1016/j.bbrc.2022.06.026