Zeng Chuili, Guo Ming, Xiao Ke, Li Chenghua
State Key Laboratory for Managing Biotic and Chemical Threats to the Quality and Safety of Agro-products, Ningbo University, Ningbo, 315211, China.
Laboratory for Marine Fisheries Science and Food Production Processes, Qingdao National Laboratory for Marine Science and Technology, Qingdao, 266071, PR China.
Cell Commun Signal. 2025 Jan 7;23(1):8. doi: 10.1186/s12964-024-01993-0.
Autophagy is essential for maintaining material balance and energy circulation and plays a critical role as a regulatory mechanism in tissue regeneration. However, current studies primarily describe this phenotype, with limited exploration of its molecular mechanisms. In this study, we provided the first evidence that autophagy is required for intestinal regeneration in Apostichopus japonicus and identified a previously unrecognized regulatory mechanism involved in this process. We observed that autophagy activation was significantly associated with enhanced regeneration, and its upregulation was shown to be regulated by reactive oxygen species (ROS) bursts. Mechanistically, ROS induced the dephosphorylation of Forkhead box protein O (FoxO) through AjAKT dephosphorylation. The dephosphorylated AjFoxO translocated to the nucleus, where it bound to the promoters of AjLC3 and AjATG4, inducing their transcription. This study highlights the ROS-AjAKT-AjFoxO-AjATG4/AjLC3 pathway as a novel regulatory mechanism underlying autophagy-mediated intestinal regeneration in echinoderms, providing a reference for studying regenerative processes and cytological mechanisms in economically important echinoderms.
自噬对于维持物质平衡和能量循环至关重要,并且作为一种调节机制在组织再生中发挥关键作用。然而,目前的研究主要描述这种表型,对其分子机制的探索有限。在本研究中,我们首次提供证据表明自噬是仿刺参肠道再生所必需的,并确定了这一过程中一种以前未被认识的调节机制。我们观察到自噬激活与再生增强显著相关,并且其上调被证明受活性氧(ROS)爆发调节。机制上,ROS通过仿刺参AKT(AjAKT)去磷酸化诱导叉头框蛋白O(FoxO)去磷酸化。去磷酸化的仿刺参FoxO(AjFoxO)易位至细胞核,在那里它与仿刺参微管相关蛋白轻链3(AjLC3)和仿刺参自噬相关蛋白4(AjATG4)的启动子结合,诱导它们的转录。本研究突出了ROS-AjAKT-AjFoxO-AjATG4/AjLC3途径作为棘皮动物中自噬介导的肠道再生潜在的一种新调节机制,为研究经济上重要的棘皮动物的再生过程和细胞学机制提供了参考。