Almost all currently available treatments for inflammatory bowel disease (IBD) act by inhibiting inflammation, often blocking specific inflammatory molecules. However, given the infectious and neoplastic disease burden associated with chronic immunosuppressive therapy, the goal of attaining mucosal healing without immunosuppression is attractive. The absence of treatments that directly promote mucosal healing and regeneration in IBD could be linked to the lack of understanding of the underlying pathways. The range of potential strategies to achieve mucosal healing is diverse. However, the targeting of regenerative mechanisms has not yet been achieved for IBD. Stem cells provide hope as a regenerative treatment and are used in limited clinical situations. Growth factors are available for the treatment of short bowel syndrome but have not yet been applied in IBD. The therapeutic application of organoid culture and stem cell therapy to generate new intestinal tissue could provide a novel mechanism to restore barrier function in IBD. Furthermore, blocking key effectors of barrier dysfunction (such as MLCK or damage-associated molecular pattern molecules) has shown promise in experimental IBD. Here, we review the diversity of molecular targets available to directly promote mucosal healing, experimental models to identify new potential pathways and some of the anticipated potential therapies for IBD.

几乎所有目前可用的炎症性肠病 (IBD) 治疗方法都是通过抑制炎症发挥作用，通常是阻断特定的炎症分子。然而，考虑到与慢性免疫抑制治疗相关的传染性和肿瘤性疾病负担，在没有免疫抑制的情况下实现粘膜愈合的目标很有吸引力。缺乏直接促进 IBD 粘膜愈合和再生的治疗方法可能与缺乏对潜在途径的了解有关。实现粘膜愈合的潜在策略范围多种多样。然而，IBD 尚未实现再生机制的靶向。干细胞作为再生治疗提供了希望，并在有限的临床情况下使用。生长因子可用于治疗短肠综合征，但尚未应用于 IBD。类器官培养和干细胞治疗产生新肠组织的治疗应用可以提供恢复 IBD 屏障功能的新机制。此外，阻断屏障功能障碍的关键效应物（如 MLCK 或损伤相关分子模式分子）已在实验性 IBD 中显示出希望。在这里，我们回顾了可用于直接促进粘膜愈合的分子靶点的多样性、确定新的潜在途径的实验模型以及一些预期的 IBD 潜在疗法。阻断屏障功能障碍的关键效应物（如 MLCK 或损伤相关分子模式分子）已在实验性 IBD 中显示出前景。在这里，我们回顾了可用于直接促进粘膜愈合的分子靶点的多样性、确定新的潜在途径的实验模型以及一些预期的 IBD 潜在疗法。阻断屏障功能障碍的关键效应物（如 MLCK 或损伤相关分子模式分子）已在实验性 IBD 中显示出前景。在这里，我们回顾了可用于直接促进粘膜愈合的分子靶点的多样性、确定新的潜在途径的实验模型以及一些预期的 IBD 潜在疗法。