中枢神经系统(CNS)

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Cell:黄鹏翔/江建森团队揭开甲状腺激素的大脑转运之谜
生物世界· 2025-07-18 04:06
Core Insights - The article discusses the critical role of thyroid hormone transport to the brain for normal neural development, mediated by the transport proteins MCT8 and OATP1C1 [2][3]. Group 1: Research Findings - A recent study published in the journal Cell by researchers from Baylor College of Medicine and the National Institutes of Health provides structural insights into the transport mechanisms of thyroid hormones via MCT8 and OATP1C1 [4][5]. - The study utilized cryo-electron microscopy to analyze the structures of MCT8 and OATP1C1 in complex with active thyroid hormones T3 and its precursor T4, achieving resolutions of 2.9 Å and 2.3 Å respectively [7]. - Key findings include the high transport specificity of MCT8 for thyroid hormones, the selective transport mechanism of OATP1C1 for thyroxine, and the discovery of a conserved extracellular regulatory site in OATP1C1 that can be allosterically inhibited by E1G [9][11].
修改教科书的发现:华人学者Nature论文首次证实,健康大脑中竟存在T细胞,来自肠道和脂肪,帮助调控饮食行为
生物世界· 2025-05-31 03:53
Core Viewpoint - The research published by Yale University confirms the presence of T cells in the healthy brains of mice and humans, specifically in the subfornical organ (SFO), indicating that T cells can reside in the brain under normal conditions, contrary to previous beliefs about the blood-brain barrier and immune cell isolation [3][11]. Group 1: Research Findings - The study reveals that T cells in the SFO are enriched and play a crucial role in monitoring gut and fat tissue information, which is essential for regulating feeding and behavior [3][11]. - T cells in the SFO are distinct from those in the meninges, as they express proteins like CXCR6 that allow them to remain in brain tissue and secrete immune signaling proteins such as IFNγ [8][11]. - The research indicates a relationship between dietary habits and the quantity of T cells in the brain, with high-fat diets leading to an increase in T cells in both fat tissue and the brain [8][9]. Group 2: Mechanisms of Interaction - The study demonstrates that fasting increases T cell numbers in the brain while decreasing them in fat tissue, suggesting that dietary intake can dynamically regulate T cell migration to the central nervous system [9][11]. - Antibiotic intervention to deplete gut microbiota resulted in a significant reduction of T cells in the brain, indicating that gut microbiota may influence immune cell homeostasis in the central nervous system [9][11]. - The presence of T cells in the brain is linked to feeding behavior, as T cell-deficient mice took longer to find food when hungry compared to normal mice, highlighting their role in foraging and eating behaviors [9][11].
Cell子刊:揭开FGF21为何能够逆转严重脂肪肝
生物世界· 2025-05-14 03:21
Core Viewpoint - Metabolic dysfunction-associated steatotic liver disease (MASLD) and its progressive form, metabolic dysfunction-associated steatohepatitis (MASH), are increasingly serious public health burdens with limited treatment options. Recent studies indicate that fibroblast growth factor-21 (FGF21) analogs can significantly improve MASH, although the mechanisms remain unclear [2]. Group 1 - A study published by researchers from the University of Iowa in Cell Metabolism demonstrates that FGF21 reverses MASH through coordinated actions on the central nervous system (CNS) and liver [3]. - The research team established that FGF21 exerts beneficial metabolic effects to reverse MASH by independently reducing liver triglyceride and cholesterol levels through different mechanisms [5]. - FGF21 signaling directly acts on glutamatergic neurons in the CNS, stimulating the reduction of liver triglycerides and reversing fibrosis, while also directly signaling liver cells to lower cholesterol levels [6][8]. Group 2 - Mechanistically, FGF21 increases sympathetic nervous activity in the liver, thereby inhibiting de novo lipogenesis [7]. - The core findings of the study include that FGF21 can reverse diet-induced MASH, directly signals the CNS to lower liver triglyceride levels and fibrosis, signals liver cells to reduce cholesterol during MASH, and enhances liver sympathetic nervous activity while decreasing de novo lipogenesis [8]. - Overall, these findings provide a promising drug target and new insights for the treatment of MASH [10].