EPISODE · Feb 9, 2026 · 16 MIN
490-长新冠胃肠后遗症的过氧化物酶修复机制
from 聊聊Sci
这项研究揭示了长新冠（long COVID）引发持续性胃肠道症状的分子机制，指出肠道病毒库是导致后遗症的关键。研究发现，新冠病毒的刺突蛋白（Spike）会直接干扰肠道内的极长链脂肪酸（VLCFA）代谢，进而抑制PPAR信号通路并导致过氧化物酶体数量减少。这种代谢紊乱阻碍了肠道干细胞的分化与上皮组织的修复，引发慢性腹泻、肠道炎症及菌群失调。通过在小鼠和果蝇模型中的实验，研究证实使用苯丁酸钠（NaPB）或非诺贝特等药物可以恢复过氧化物酶体功能，有效缓解消化系统症状。这些发现不仅阐明了病毒如何长期破坏肠道稳态，还为治疗长新冠肠道并发症提供了潜在的临床方案。References: Wang M, Chen Y, Guo M, et al. Impaired VLCFA-peroxisome-mediated intestinal epithelial repair causes gastrointestinal sequelae of long COVID[J]. Developmental Cell, 2026.前往小宇宙评论区与主播互动
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490-长新冠胃肠后遗症的过氧化物酶修复机制
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