Abstract：
Accumulating evidence has shown that cell dedifferentiation or reprogramming is a pivotal procedure for animals to deal with injury and promote endogenous tissue repair. Tissue damage is a critical factor that triggers cell dedifferentiation or reprogramming in vivo. By contrast, microenvironmental changes, including the loss of stem cells, hypoxia, cell senescence, inflammation and immunity, caused by tissue damage can return cells to an unstable state. If the wound persists in the long‑term due to chronic damage, then dedifferentiation or reprogramming of the surrounding cells may lead to carcinogenesis. In recent years, extensive research has been performed investigating cell dedifferentiation or reprogramming in vivo, which can have significant implications for wound repair, treatment and prevention of cancer in the future. The current review summarizes the molecular events that are known to drive cell dedifferentiation directly following tissue injury and the effects of epigenetic modification on dedifferentiation or reprogramming in vivo. In addition, the present review explores the intracellular mechanism of endogenous tissue repair and its relationship with cancer, which is essential for balancing the risk between tissue repair and malignant transformation after injury.
摘要：
越来越多的证据表明，细胞去分化或重编程是动物处理损伤和促进内源性组织修复的关键过程。组织损伤是体内触发细胞去分化或重编程的关键因素。相比之下,微环境变化,包括干细胞的损失，缺氧,细胞衰老,炎症和免疫力，由组织损伤引起的细胞可以返回到不稳定的状态。如果伤口由于慢性损伤而长期持续存在，然后去分化或周围细胞的重新编程可能导致癌变。近年来,已经进行了广泛的研究，研究体内细胞去分化或重编程，这对伤口修复有重大影响，未来癌症的治疗和预防。本综述总结了已知在组织损伤后直接驱动细胞去分化的分子事件以及表观遗传修饰对体内去分化或重编程的影响。此外,本综述探讨内源性组织修复的细胞内机制及其与癌症的关系，这对于平衡损伤后组织修复和恶性转化之间的风险至关重要。
