Targeting adipose tissue to tackle NASH: SPARCL1 as an emerging player

Nonalcoholic steatohepatitis (NASH) is a leading cause of chronic liver disease, affecting 1.5%-6.5% of the world population. Currently, there are no FDA-approved drugs to treat this disease. Accumulating evidence suggests that metabolically hazardous visceral fat contributes to NASH progression by...

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Bibliographic Details
Published in:The Journal of clinical investigation 2021-10, Vol.131 (20)
Main Authors: Rodrigues, Robim M, Guan, Yukun, Gao, Bin
Format: Article
Language:English
Subjects:
Adipose Tissue
Animals
Calcium-Binding Proteins
Cysteine
Extracellular Matrix Proteins
Intra-Abdominal Fat
Mice
Non-alcoholic Fatty Liver Disease - drug therapy
Osteonectin
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Summary:Nonalcoholic steatohepatitis (NASH) is a leading cause of chronic liver disease, affecting 1.5%-6.5% of the world population. Currently, there are no FDA-approved drugs to treat this disease. Accumulating evidence suggests that metabolically hazardous visceral fat contributes to NASH progression by releasing fatty acids and proinflammatory mediators. Therefore, targeting adipose tissue to reduce adipose inflammation may provide an effective strategy to treat NASH. Another strategy is to target specific inflammatory mediators that are produced by adipose tissue and contribute to NASH progression. In this issue of the JCI, Liu, Xiang, et al. demonstrate that secreted protein acidic and rich in cysteine-like protein 1 (SPARCL1) was highly upregulated in adipose tissue and played a role in exacerbating NASH progression in a mouse model of NASH. Thus, inhibition of SPARCL1 may provide another attractive strategy to tackle NASH.
ISSN:1558-8238
0021-9738
1558-8238
DOI:10.1172/JCI153640