以色列Weizmann研究所的研究人员发现了一类称为DARE细胞的特殊细胞，这些细胞能够启动程序性细胞死亡过程但最终存活下来1。研究显示，DARE细胞在48小时内修复了几乎一半的受损组织1。这一机制基于补偿性增殖，通过DARE细胞与NARE细胞之间的负反馈循环来防止过度生长1。
值得注意的是，DARE细胞的后代对细胞死亡的抵抗力是原始组织中细胞的7倍1。在重复辐射实验中，第二次照射导致的死亡细胞数仅为第一次的一半，表明存活细胞的后代获得了更强的抵抗力1。研究还揭示了一个意外发现：通常已知会摧毁细胞的Caspase酶实际上可以帮助某些细胞变得对死亡更具抵抗力1。
这一发现发表在2025年的《自然通讯》期刊上1，揭示了受损组织快速重建的分子机制。然而，研究人员也指出，这一机制可能同时解释了为何某些癌症在治疗后会复发并显示出更强的抵抗性1。
Researchers at the Weizmann Institute have identified a distinctive cell population called DARE cells—cells that initiate programmed cell death but ultimately survive the process—capable of rapidly reconstructing damaged tissue.1 These cells repaired nearly half of damaged tissue within 48 hours,1 and their offspring displayed seven times greater resistance to cell death compared to cells in the original tissue.1
The discovery reveals the molecular mechanisms underlying compensatory proliferation, a process where surviving cells multiply to restore tissue structure. Notably, caspase enzymes, proteins typically known to destroy cells, were found to help certain cells become more resistant to death.1 When tissue was subjected to a second round of radiation, the number of cell deaths was only half that of the first exposure, indicating that the offspring of surviving cells had acquired enhanced resistance.1 A negative feedback loop exists between DARE cells and NARE cells to prevent excessive growth.1
These findings, published in Nature Communications in 2025,1 offer important insights into tissue regeneration but also raise concerns about cancer treatment. The same mechanisms that enable DARE cells to survive and proliferate may explain why certain cancers relapse after treatment with increased resistance to therapy.1
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