188 research outputs found
Novel Strategies Targeting Obesity and Metabolic Diseases
No full textThis eBook is a collection of articles from a Frontiers Research Topic. Frontiers Research Topics are very popular trademarks of the Frontiers Journals Series: they are collections of at least ten articles, all centered on a particular subject. With their unique mix of varied contributions from Original Research to Review Articles, Frontiers Research Topics unify the most influential researchers, the latest key findings and historical advances in a hot research area! Find out more on how to host your own Frontiers Research Topic or contribute to one as an author by contacting the Frontiers Editorial Office: frontiersin.org/about/contac
Adipocyte Death Preferentially Induces Liver Injury and Inflammation Through the Activation of Chemokine (C‐C Motif) Receptor 2‐Positive Macrophages and Lipolysis
No full textAdipocyte death occurs under various physiopathological conditions, including obesity and alcohol drinking, and can trigger organ damage particularly in the liver, but the underlying mechanisms remain obscure. To explore these mechanisms, we developed a mouse model of inducible adipocyte death by overexpressing the human CD59 (hCD59) on adipocytes (adipocyte-specific hCD59 transgenic mice). Injection of these mice with intermedilysin (ILY), which rapidly lyses hCD59 expressing cells exclusively by binding to the hCD59 but not mouse CD59, resulted in the acute selective death of adipocytes, adipose macrophage infiltration, and elevation of serum free fatty acid (FFA) levels. ILY injection also resulted in the secondary damage to multiple organs with the strongest injury observed in the liver, with inflammation and hepatic macrophage activation. Mechanistically, acute adipocyte death elevated epinephrine and norepinephrine levels and activated lipolysis pathways in adipose tissue in a chemokine (C-C motif) receptor 2-positive (CCR2(+)) macrophage-dependent manner, which was followed by FFA release and lipotoxicity in the liver. Additionally, acute adipocyte death caused hepatic CCR2(+) macrophage activation and infiltration, further exacerbating liver injury. Conclusion: Adipocyte death predominantly induces liver injury and inflammation, which is probably due to the superior sensitivity of hepatocytes to lipotoxicity and the abundance of macrophages in the liver.
Interleukin-22 in the pathogenesis and potential treatment of liver diseases
No full textInterleukin (IL)-22, a member of the IL-10 cytokine family, plays critical roles in tissue repair and host defense. IL-22 binds to its hetereodimeric receptor (R) composed of IL-22R1 and IL-10R2 and activates downstream signaling, including Signal transducer and activator of transcription 3 (STAT3) pathways. IL-22 promotes the expression of survival genes in a STAT3-dependent manner. IL-22R1 expression is restricted mainly in epithelial cells while IL-10R2 is ubiquitously expressed in almost all cell types. In the liver, IL-22R1 is expressed in hepatocytes, liver progenitor cells, hepatic stellate cells and liver cancer cells. IL-22 protects the liver in various liver damage models and promotes liver regeneration after liver injury. IL-22 also helps to resolve liver fibrosis by inducing hepatic stellate cell senescence. IL-22 is considered a pro-inflammatory cytokine in viral hepatitis although it does not directly act on immune cells. IL-22 is reported to be involved in the development of liver cancer and in regulating energy metabolism. Studies on IL-22 in liver inflammation, injury and repair will provide valuable information to clarify IL-22 as a potential candidate for treating liver injury and fibrosis. Keywords: Interleukin (IL)-22, Liver injury, Liver repair, Signal transducer and activator of transcription 3 (STAT3
The study of temperature measurement on optical fiber in OPGW based on stimulated Brillouin scattering
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