Extramedullary hematopoiesis (EMH) is the expansion and differentiation of hematopoietic stem and progenitor cells outside of the bone marrow. In postnatal life, as a compensatory mechanism for ineffective hematopoiesis of the bone marrow, pathological EMH is triggered by hematopoietic disorders, insufficient hematopoietic compensation, and other pathological stress conditions, such as infection, advanced tumors, anemia, and metabolic stress. Pathological EMH has been reported in many organs, and the sites of pathological EMH may be related to reactivation of the embryonic hematopoietic structure in these organs. As a double-edged sword (blood and immune cell supplementation as well as clinical complications), pathological EMH has been widely studied in recent years. In particular, pathological EMH induced by late-stage tumors contributes to tumor immunosuppression. Thus, a deeper understanding of the mechanism of pathological EMH may be conducive to the development of therapies against the pathological processes that induce EMH. This article reviews the recent progress of research on the cellular and molecular mechanisms of pathological EMH in specific diseases.

髓外造血（EMH）是造血干细胞和祖细胞在骨髓外的扩增和分化。在出生后的生活中，作为骨髓无效造血的代偿机制，造血障碍、造血代偿不足以及其他病理应激条件（如感染、晚期肿瘤、贫血和代谢应激）会引发病理性EMH。许多器官都有病理性EMH的报道，病理性EMH发生的部位可能与这些器官中胚胎造血结构的重新激活有关。作为一把双刃剑（血液和免疫细胞的补充以及临床并发症），病理EMH近年来得到了广泛的研究。特别是，晚期肿瘤诱导的病理性 EMH 有助于肿瘤免疫抑制。因此，更深入地了解病理性 EMH 的机制可能有助于开发针对诱发 EMH 的病理过程的疗法。本文综述了特定疾病病理EMH的细胞分子机制的研究进展。