AI Article Synopsis

  • NAFLD is a serious chronic disease linked to high mortality and significant global healthcare costs.
  • The liver's immune cells, such as macrophages and NK cells, become activated by damage signals, triggering inflammation.
  • The STING pathway is essential for initiating immune responses and recent research suggests its altered activity may contribute to liver diseases like NAFLD, leading to studies on potential inhibitors and agonists targeting STING.

Article Abstract

Non-alcoholic fatty liver disease (NAFLD), an important chronic disease, is one of the major causes of high mortality and creates a substantial financial burden worldwide. The various immune cells in the liver, including macrophages, NK cells, dendritic cells, and the neutrophils involved in the innate immune response, trigger inflammation after recognizing the damage signaled from infection or injured cells and tissues. The stimulator of interferon genes (STING) is a critical molecule that binds to the cyclic dinucleotides (CDNs) generated by the cyclic GMP-AMP synthase (cGAS) to initiate the innate immune response against infection. Previous studies have demonstrated that the cGAS-STING pathway plays a critical role in inflammatory, auto-immune, and anti-viral immune responses. Recently, studies have focused on the role of STING in liver diseases, the results implying that alterations in its activity may be involved in the pathogenesis of liver disorders. Here, we summarize the function of STING in the development of NAFLD and present the current inhibitors and agonists targeting STING.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9611148PMC
http://dx.doi.org/10.3390/ph15101241DOI Listing

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