Publications by authors named "Zi-Ying Liu"
Article Synopsis
- Osteoclast (OC) over-activation due to inflammation is linked to bone loss, and the study investigates the role of the CD163/TWEAK/Fn14 signaling pathway in this process.
- Researchers compared CD163-deficient mice to normal mice, analyzed the effects of CD163 and TWEAK levels in bone marrow, and studied the impacts of rCD163 supplementation and TWEAK/Fn14 blockade on bone mass.
- Results showed that CD163 deficiency led to reduced bone mass and increased OC presence; targeting the CD163/TWEAK/Fn14 axis may offer a new therapy for inflammatory bone loss by influencing osteoclast activity.
Objective: About 10% of patients after cardiopulmonary bypass (CPB) would undergo acute liver injury, which aggravated the mortality of patients. Ac2-26 has been demonstrated to ameliorate organic injury by inhibiting inflammation. The present study aims to evaluate the effect and mechanism of Ac2-26 on acute liver injury after CPB.
View Article and Find Full Text PDFBackground: Cardiopulmonary bypass (CPB) results in brain injury, which is primarily caused by inflammation. Ac2-26 protects against ischemic or hemorrhage brain injury. The present study was to explore the effect and mechanism of Ac2-26 on brain injury in CPB rats.
View Article and Find Full Text PDFCNTF induces Clcf1 in astrocytes to promote the differentiation of oligodendrocyte precursor cells.
Biochem Biophys Res Commun
December 2022
Article Synopsis
- - Neural stem cells (NSCs) are crucial for regeneration in the central nervous system but face challenges because of a harsh microenvironment, limiting their effectiveness in therapies.
- - Research indicates that NSCs engineered to overexpress ciliary neurotrophic factor (CNTF) show improved remyelination effects, but the exact mechanism is not fully understood.
- - The study reveals that CNTF-NSCs can induce astrocytes to produce cardiotrophin-like cytokine 1 (Clcf1), which promotes the differentiation of oligodendrocyte precursor cells, highlighting Clcf1 as a potential therapeutic target for demyelinating diseases.