Publications by authors named "Luolun Dong"
Wnt5a promotes Kupffer cell activation in trichloroethylene-induced immune liver injury.
Toxicol Ind Health
February 2025
Article Synopsis
- Trichloroethylene (TCE) exposure can lead to a condition called trichloroethylene hypersensitivity syndrome (THS), but the mechanisms behind associated liver injuries remain unclear.
- This study investigated the role of Wnt5a and c-Jun N-terminal kinase (JNK) in liver damage caused by TCE using a sensitization model in mice, revealing that TCE exposure increased Wnt5a/JNK activity in the liver.
- Inhibiting Wnt5a and JNK lessened liver injury by reducing Kupffer cell activation and suppressing inflammatory responses, suggesting potential therapeutic approaches for managing TCE-induced liver damage.
In specific pathological conditions, addressing liver injury may yield favorable effects on renal function through the phenomenon of liver-kidney crosstalk. Mitochondrial DNA (mtDNA) possesses the capability to trigger downstream pathways of inflammatory cytokines, ultimately leading to immune-mediated organ damage. Consequently, understanding the intricate molecular mechanisms governing mtDNA involvement in diseases characterized by liver-kidney crosstalk is of paramount significance.
View Article and Find Full Text PDFWe 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 plays an important regulatory role in macrophage polarization. In the present study, we demonstrated that elevated levels of oxidative stress in hepatocytes mediate the release of mtDNA into the bloodstream, leading to the activation of TLR9 in macrophages to regulate macrophage polarization.
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