| First Author | Jiao J | Year | 2022 |
| Journal | Am J Pathol | Volume | 192 |
| Issue | 12 | Pages | 1745-1762 |
| PubMed ID | 36174680 | Mgi Jnum | J:334236 |
| Mgi Id | MGI:7407790 | Doi | 10.1016/j.ajpath.2022.09.002 |
| Citation | Jiao J, et al. (2022) Expression of STING Is Increased in Monocyte-Derived Macrophages and Contributes to Liver Inflammation in Hepatic Ischemia-Reperfusion Injury. Am J Pathol 192(12):1745-1762 |
| abstractText | Ischemia/reperfusion (I/R) injury, aggravated by innate immune cell-mediated inflammatory response, is a major problem in liver transplantation. Stimulator of interferon gene (STING) is a crucial regulatory signaling molecule in the DNA-sensing pathway, and its activation can produce strong innate immunity. However, the STING-mediated innate immune pathway in hepatic I/R injury has not been fully elucidated. In this study, we first examined the STING expression changes in the liver tissues of mice after hepatic I/R injury by using quantitative polymerase chain reaction and Western blot assays. We then investigated the role of STING in I/R injury by using a murine hepatic I/R model. STING up-regulation in mouse liver tissues in response to I/R injury and STING deficiency in myeloid cells was found to significantly ameliorate I/R-induced liver injury and inflammatory responses. STING inhibitors were also able to ameliorate hepatic I/R injury. Mechanically, STING may have a protective effect on hepatic I/R injury by the inhibition of hypoxia-inducible factor-1 alpha and enhancement of phosphorylated AMP-activated protein kinase to reduce macrophage activation. These findings show the potential regulatory effects of STING in hepatic I/R and suggest a new method for clinical protection of hepatic I/R injury. |
