@article{ref1,
title="STING deficiency protects against wasp venom-induced acute kidney injury",
journal="Inflammation research : official journal of the European Histamine Research Society",
year="2023",
author="Lv, Ying and Lu, Li and Yu, Fanglin and Gao, Zhao and Yuan, Hai and Hu, Fengqi",
volume="ePub",
number="ePub",
pages="ePub-ePub",
abstract="OBJECTIVE: Recent evidence suggests a key role of the inflammatory responses in wasp venom-induced acute kidney injury (AKI). However, the potential regulatory mechanisms underlying the inflammatory responses in wasp venom-induced AKI remain unclear. STING reportedly plays a critical role in other AKI types and is associated with inflammatory responses and diseases. We aimed to investigate the involvement of STING in inflammatory responses associated with wasp venom-induced AKI. <br><br>METHODS: The role of the STING signaling pathway in wasp venom-induced AKI was studied in vivo using a mouse model of wasp venom-induced AKI with STING knockout or pharmacological inhibition and in vitro using human HK2 cells with STING knockdown. <br><br>RESULTS: STING deficiency or pharmacological inhibition markedly ameliorated renal dysfunction, inflammatory responses, necroptosis, and apoptosis in wasp venom-induced AKI in mice. Moreover, STING knockdown in cultured HK2 cells attenuated the inflammatory response, necroptosis, and apoptosis induced by myoglobin, the major pathogenic factor in wasp venom-induced AKI. Urinary mitochondrial DNA upregulation has also been observed in patients with wasp venom-induced AKI. <br><br>CONCLUSIONS: STING activation mediates the inflammatory response in wasp venom-induced AKI. This may offer a potential therapeutic target for the management of wasp venom-induced AKI.<p /> <p>Language: en</p>",
language="en",
issn="1023-3830",
doi="10.1007/s00011-023-01749-5",
url="http://dx.doi.org/10.1007/s00011-023-01749-5"
}