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http://dx.doi.org/10.1186/s13054-020-03383-7 | DOI Listing |
J Cardiovasc Transl Res
January 2025
Department of Vascular and Endovascular Surgery, Changzheng Hospital, Affiliated to the Naval Medical University, Shanghai, 200003, China.
CHI3L1 is strongly associated with atherosclerosis, but its role in macrophages remains unknown. In this study, we observed a significant up-regulation of CHI3L1 in both carotid plaques and serum of symptomatic patients, and demonstrated that CHI3L1 impairs the efferocytosis of macrophages by down-regulating crucial efferocytic mediator MFGE8 through inhibiting ATF2, which binds directly to the enhancer of MFGE8. In human plaques, we observed a negative correlation between CHI3L1 expression and both ATF2 and MFGE8 levels, further proved their involvement in plaque destabilization.
View Article and Find Full Text PDFBiochem Biophys Rep
March 2025
Genis hf, Reykjavik, Iceland.
The chitinase-like protein YKL-40 (CHI3L1) has been implicated in the pathophysiology of inflammation and cancer. Recent studies highlight the growing interest in targeting and blocking the activity of YKL-40 to treat cancer. Some of those targeting-strategies have been developed to directly block the heparin-affinity of YKL-40 with promising results.
View Article and Find Full Text PDFCells
December 2024
Department of Neurology, Medical University of Lodz, Kosciuszki Street 4, 90-419 Lodz, Poland.
Multiple sclerosis (MS) is a chronic demyelinating disease of the central nervous system (CNS) with a complex and not fully understood etiopathological background involving inflammatory and neurodegenerative processes. CHI3L1 has been implicated in pathological conditions such as inflammation, injury, and neurodegeneration, and is likely to play a role in the physiological development of the CNS. CHI3L1 is primarily produced by CNS macrophages, microglia, and activated astrocytes.
View Article and Find Full Text PDFJ Orthop Surg Res
December 2024
Associated Tissue Bank, Faculty of Medicine, P.J. Safarik University and L. Pasteur University Hospital in Kosice, Tr. SNP 1, Kosice, 04011, Slovakia.
Int J Mol Sci
November 2024
Aging Brain and Memory Clinic, Department of Neuroscience "Rita Levi-Montalcini", University of Torino, 10126 Torino, Italy.
The identification of neuroinflammation as a critical factor in Alzheimer's disease (AD) has expanded the focus of research beyond amyloid-β and tau pathology. The neuroinflammatory fluid biomarkers GFAP, sTREM2, and YKL-40 have gained attention for their potential in early detection and monitoring of disease progression. Plasma GFAP has demonstrated promise in predicting the conversion from mild cognitive impairment to AD dementia, while sTREM2 highlights microglial activation, although there are conflicting results regarding its dynamics in AD pathogenesis.
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