Tanycytes, specialized ependymal cells located in the hypothalamus, play a crucial role in the generation of new neurons that contribute to the neural circuits responsible for regulating the systemic energy balance. T...Tanycytes, specialized ependymal cells located in the hypothalamus, play a crucial role in the generation of new neurons that contribute to the neural circuits responsible for regulating the systemic energy balance. The precise coordination of the gene networks controlling neurogenesis in naive and mature tanycytes is essential for maintaining homeostasis in adulthood. However, our understanding of the molecular mechanisms and signaling pathways that govern the proliferation and differentiation of tanycytes into neurons remains limited. This article aims to review the recent advancements in research into the mechanisms and functions of tanycyte-derived neurogenesis. Studies employing lineage-tracing techniques have revealed that the neurogenesis specifically originating from tanycytes in the hypothalamus has a compensatory role in neuronal loss and helps maintain energy homeostasis during metabolic diseases. Intriguingly,metabolic disorders are considered early biomarkers of Alzheimer's disease. Furthermore,the neurogenic potential of tanycytes and the state of newborn neurons derived from tanycytes heavily depend on the maintenance of mild microenvironments, which may be disrupted in Alzheimer's disease due to the impaired blood–brain barrier function.However, the specific alterations and regulatory mechanisms governing tanycyte-derived neurogenesis in Alzheimer's disease remain unclear. Accumulating evidence suggests that tanycyte-derived neurogenesis might be impaired in Alzheimer's disease, exacerbating neurodegeneration. Confirming this hypothesis, however, poses a challenge because of the lack of long-term tracing and nucleus-specific analyses of newborn neurons in the hypothalamus of patients with Alzheimer's disease. Further research into the molecular mechanisms underlying tanycyte-derived neurogenesis holds promise for identifying small molecules capable of restoring tanycyte proliferation in neurodegenerative diseases. This line of investigation could provide valuable insights into potential therapeutic strategies for Alzheimer's disease and related conditions.展开更多
目的探讨甲状腺功能减退患者应用非诺贝特发生横纹肌溶解的临床特征,为临床安全用药提供参考。方法分享1例甲状腺功能减退患者应用非诺贝特发生横纹肌溶解的临床案例,检索国内外报道的不良反应文献,归纳总结其发生特点。结果25岁女性,...目的探讨甲状腺功能减退患者应用非诺贝特发生横纹肌溶解的临床特征,为临床安全用药提供参考。方法分享1例甲状腺功能减退患者应用非诺贝特发生横纹肌溶解的临床案例,检索国内外报道的不良反应文献,归纳总结其发生特点。结果25岁女性,高脂血症合并甲状腺功能减退,应用非诺贝特12 d后发生横纹肌溶解症,横纹肌溶解发生前监测甲功TSH高,不良反应发生后停用非诺贝特并积极补液同时碱化尿液,症状好转出院。文献检索到11例甲减患者应用非诺贝特发生横纹肌溶解的报道,年龄25~68岁,男女比例1∶2,除3例甲状腺功能不详外,6例为甲状腺功能减退,2例游离甲状腺素(FT4)在正常低限。9例非诺贝特剂量符合说明书,3例剂量超过说明书推荐剂量。药物不良反应(adverse drug reaction,ADR)多发生于用药后3~60 d。10例痊愈,2例好转。结论甲状腺功能减退可能是非诺贝特发生横纹肌溶解的风险因素,甲状腺功能减退患者用药前应监测甲状腺功能,并调整治疗使FT4和TSH控制在正常范围。展开更多
基金supported by the National Natural Science Foundation of China,Nos.31871477,32170971 (both to SQ)the Qing-Feng Scholar Research Foundation of Shanghai Medical College,Fudan University,No.QF2212 (to HT)。
文摘Tanycytes, specialized ependymal cells located in the hypothalamus, play a crucial role in the generation of new neurons that contribute to the neural circuits responsible for regulating the systemic energy balance. The precise coordination of the gene networks controlling neurogenesis in naive and mature tanycytes is essential for maintaining homeostasis in adulthood. However, our understanding of the molecular mechanisms and signaling pathways that govern the proliferation and differentiation of tanycytes into neurons remains limited. This article aims to review the recent advancements in research into the mechanisms and functions of tanycyte-derived neurogenesis. Studies employing lineage-tracing techniques have revealed that the neurogenesis specifically originating from tanycytes in the hypothalamus has a compensatory role in neuronal loss and helps maintain energy homeostasis during metabolic diseases. Intriguingly,metabolic disorders are considered early biomarkers of Alzheimer's disease. Furthermore,the neurogenic potential of tanycytes and the state of newborn neurons derived from tanycytes heavily depend on the maintenance of mild microenvironments, which may be disrupted in Alzheimer's disease due to the impaired blood–brain barrier function.However, the specific alterations and regulatory mechanisms governing tanycyte-derived neurogenesis in Alzheimer's disease remain unclear. Accumulating evidence suggests that tanycyte-derived neurogenesis might be impaired in Alzheimer's disease, exacerbating neurodegeneration. Confirming this hypothesis, however, poses a challenge because of the lack of long-term tracing and nucleus-specific analyses of newborn neurons in the hypothalamus of patients with Alzheimer's disease. Further research into the molecular mechanisms underlying tanycyte-derived neurogenesis holds promise for identifying small molecules capable of restoring tanycyte proliferation in neurodegenerative diseases. This line of investigation could provide valuable insights into potential therapeutic strategies for Alzheimer's disease and related conditions.
文摘目的探讨甲状腺功能减退患者应用非诺贝特发生横纹肌溶解的临床特征,为临床安全用药提供参考。方法分享1例甲状腺功能减退患者应用非诺贝特发生横纹肌溶解的临床案例,检索国内外报道的不良反应文献,归纳总结其发生特点。结果25岁女性,高脂血症合并甲状腺功能减退,应用非诺贝特12 d后发生横纹肌溶解症,横纹肌溶解发生前监测甲功TSH高,不良反应发生后停用非诺贝特并积极补液同时碱化尿液,症状好转出院。文献检索到11例甲减患者应用非诺贝特发生横纹肌溶解的报道,年龄25~68岁,男女比例1∶2,除3例甲状腺功能不详外,6例为甲状腺功能减退,2例游离甲状腺素(FT4)在正常低限。9例非诺贝特剂量符合说明书,3例剂量超过说明书推荐剂量。药物不良反应(adverse drug reaction,ADR)多发生于用药后3~60 d。10例痊愈,2例好转。结论甲状腺功能减退可能是非诺贝特发生横纹肌溶解的风险因素,甲状腺功能减退患者用药前应监测甲状腺功能,并调整治疗使FT4和TSH控制在正常范围。
