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View article: Adverse Event Assessment of Upadacitinib: A Pharmacovigilance Study Based on the <scp>FAERS</scp> Database
Adverse Event Assessment of Upadacitinib: A Pharmacovigilance Study Based on the <span>FAERS</span> Database Open
Purpose Upadacitinib, a Janus kinase (JAK) inhibitor, has been approved by the FDA to treat various autoimmune conditions. This study assessed its adverse events by analyzing reports from the FDA Adverse Event Reporting System (FAERS). Met…
View article: Hepatocyte mitochondrial DNA mediates macrophage immune response in liver injury induced by trichloroethylene
Hepatocyte mitochondrial DNA mediates macrophage immune response in liver injury induced by trichloroethylene Open
We have previously shown that excessive activation of macrophage proinflammatory activity plays a key role in TCE-induced immune liver injury, but the mechanism of polarization is unclear. Recent studies have shown that TLR9 activation pla…
View article: Trichloroethylene induced hepatic injury via M1 macrophage polarization through KDM4A associated with the Wnt/β-catenin pathway in vitro and in vivo
Trichloroethylene induced hepatic injury via M1 macrophage polarization through KDM4A associated with the Wnt/β-catenin pathway in vitro and in vivo Open
Background & Aims: Trichloroethylene (TCE) is a commonly used organic solvent in industry. Our previous studies have found that TCE can cause liver injury accompanied by macrophage polarization, but the specific mechanism is unclear. The e…
View article: IP3R-dependent mitochondrial dysfunction mediates C5b-9-induced ferroptosis in trichloroethylene-caused immune kidney injury
IP3R-dependent mitochondrial dysfunction mediates C5b-9-induced ferroptosis in trichloroethylene-caused immune kidney injury Open
Patients with occupational medicamentose-like dermatitis due to trichloroethylene often suffer from immune kidney injury. Our previous study reveals that C5b-9-dependent cytosolic Ca 2+ overload-induced ferroptosis is involved in trichloro…
View article: Effects of mitochondrial reactive oxygen species-induced NLRP3 inflammasome activation on trichloroethylene-mediated kidney immune injury
Effects of mitochondrial reactive oxygen species-induced NLRP3 inflammasome activation on trichloroethylene-mediated kidney immune injury Open
This study aimed to investigate the activating mechanism of the NLRP3 inflammasome in trichloroethylene-sensitized mice. In total, 88 BALB/c female mice were used to establish the trichloroethylene (TCE)-sensitized mouse model. Some of the…
View article: C5b-9 mediates ferroptosis of tubular epithelial cells in trichloroethylene-sensitization mice
C5b-9 mediates ferroptosis of tubular epithelial cells in trichloroethylene-sensitization mice Open
View article: Wnt 5a mediated inflammatory injury of renal tubular epithelial cells dependent on calcium signaling pathway in Trichloroethylene sensitized mice
Wnt 5a mediated inflammatory injury of renal tubular epithelial cells dependent on calcium signaling pathway in Trichloroethylene sensitized mice Open
Patients with trichloroethene-induced Trichloroethylene hypersensitivity syndrome (THS) often present kidney injury. However, the role of Wnt 5a/Ca2+ pathway in renal tubular injury in Trichloroethylene (TCE) sensitized mice rem…