胚胎遗传程序因各种类型的组织损伤而被重新激活，为组织再生或疾病进展提供细胞可塑性。在紧急情况下，这些程序会修复损害，然后停止以恢复稳态。在慢性疾病中，包括炎症性疾病、纤维化和癌症，胚胎程序的长期激活会导致疾病进展和组织恶化。祖细胞身份和细胞可塑性（例如上皮间充质可塑性）的诱导是重新激活胚胎程序的关键结果。在这篇综述中，我们描述了控制重新激活的胚胎遗传程序的分子参与者、它们在疾病进展中的作用、它们的相似点和差异以及病理学中的谱系逆转，并讨论了许多器官的相关治疗和耐药机制。我们还讨论了不同疾病背景下重新激活程序的多样性。对发育和疾病之间共性的全面概述将有助于更好地理解生物学和治疗策略。© 2023。Springer Nature America, Inc.

Embryonic genetic programs are reactivated in response to various types of tissue damage, providing cell plasticity for tissue regeneration or disease progression. In acute conditions, these programs remedy the damage and then halt to allow a return to homeostasis. In chronic situations, including inflammatory diseases, fibrosis and cancer, prolonged activation of embryonic programs leads to disease progression and tissue deterioration. Induction of progenitor identity and cell plasticity, for example, epithelial-mesenchymal plasticity, are critical outcomes of reactivated embryonic programs. In this Review, we describe molecular players governing reactivated embryonic genetic programs, their role during disease progression, their similarities and differences and lineage reversion in pathology and discuss associated therapeutics and drug-resistance mechanisms across many organs. We also discuss the diversity of reactivated programs in different disease contexts. A comprehensive overview of commonalities between development and disease will provide better understanding of the biology and therapeutic strategies.© 2023. Springer Nature America, Inc.