Hepatology research : the official journal of the Japan Society of Hepatology · 2025
Involvement of the ADAMTS13-von Willebrand factor axis in acute kidney injury in mice with liver cirrhosis.
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Takami Masayoshi, Nishimura Norihisa, Kaji Kosuke, Yorioka Nobuyuki, Masuda Hiroyuki, Takaya Hiroaki, Kitagawa Koh, Sato Shinya, Namisaki Tadashi, Yoshiji Hitoshi
Аннотация
AIM: Hepatorenal syndrome-induced acute kidney injury (AKI) comprises AKI and liver cirrhosis (LC) and is a risk factor for poor prognoses of patients with LC. Decreased a disintegrin-like metalloproteinase with thrombospondin type 1 motif 13 (ADAMTS13) activity and increased von Willebrand factor (vWF) antigen levels are associated with LC progression and portal hypertension. We investigated the role of the ADAMTS13-vWF axis in AKI using an LC mouse model.
METHODS: Wild-type and ADAMTS13-deficient (Adamts13-/-) 129+Ter/Sv mice comprised the negative control and AKI groups. AKI was induced by intraperitoneal carbon tetrachloride, a single injection of a double dose of carbon tetrachloride, and lipopolysaccharide administration. Wild-type and vWF-deficient C57/B6J mice comprised a secondary animal model. Effects of ADAMTS13 alterations on liver and kidney injuries, and the role of vWF in AKI in the cirrhotic mouse model were analyzed.
RESULTS: AKI groups of wild-type and Adamts13-/- mice showed increased serum aspartate aminotransferase/alanine aminotransferase and blood urea nitrogen/creatinine levels. Significantly greater changes in Adamts13-/- mice were observed. Blood flow in the liver and kidney was significantly decreased in the AKI group of Adamts13-/- mice. The AKI group of Adamts13-/- mice also demonstrated inflammatory changes, including increased F4/80-positive cells and renal injury markers in the kidney. Oxidative stress markers were increased in Adamts13-/- mice after AKI induction. Conversely, vWF-deficient mice were protected from liver and kidney damage, and showed reduced tissue blood flow, inflammation, and oxidative stress responses.
CONCLUSION: An imbalanced ADAMTS13-vWF axis may play a critical role in AKI progression with LC.
METHODS: Wild-type and ADAMTS13-deficient (Adamts13-/-) 129+Ter/Sv mice comprised the negative control and AKI groups. AKI was induced by intraperitoneal carbon tetrachloride, a single injection of a double dose of carbon tetrachloride, and lipopolysaccharide administration. Wild-type and vWF-deficient C57/B6J mice comprised a secondary animal model. Effects of ADAMTS13 alterations on liver and kidney injuries, and the role of vWF in AKI in the cirrhotic mouse model were analyzed.
RESULTS: AKI groups of wild-type and Adamts13-/- mice showed increased serum aspartate aminotransferase/alanine aminotransferase and blood urea nitrogen/creatinine levels. Significantly greater changes in Adamts13-/- mice were observed. Blood flow in the liver and kidney was significantly decreased in the AKI group of Adamts13-/- mice. The AKI group of Adamts13-/- mice also demonstrated inflammatory changes, including increased F4/80-positive cells and renal injury markers in the kidney. Oxidative stress markers were increased in Adamts13-/- mice after AKI induction. Conversely, vWF-deficient mice were protected from liver and kidney damage, and showed reduced tissue blood flow, inflammation, and oxidative stress responses.
CONCLUSION: An imbalanced ADAMTS13-vWF axis may play a critical role in AKI progression with LC.