Aplastic anemia (AA) is an autoimmune disorder characterized by bone marrow and peripheral blood pancytopenia. Different environmental and genetical conditions could be effective in an outbreak of this disease. The exact pathogenesis of this disease, however, is still idiopathic. The present study is based on Pubmed database information (2002–2021) using the words “Aplastic Anemia,” “Hematopoietic Stem Cells niche,” “Signaling pathway,” “Cytokines,” and “Immuno cells.” In this disease, both hematopoietic stem cells and mesenchymal stromal cells are impaired, which is associated with impaired hematopoiesis and decreased hematopoietic cells. Inflammatory cytokines increase, which changes the ratio of T lymphocytes and leads to disease progression. In addition, the most common mechanism of AA is damage by the immune system, which leads to increased apoptosis in progenitor cells. We have shown in this review that the disease involves quantitative defects in stem cell numbers and qualitative abnormalities in the function of these cells and the activity of many different cellular and molecular factors can damage hematopoietic cells and the protective substrate of these cells in this disease.

中文翻译：

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再生障碍性贫血，细胞和分子方面

再生障碍性贫血 (AA) 是一种以骨髓和外周血全血细胞减少为特征的自身免疫性疾病。不同的环境和遗传条件可能对这种疾病的爆发有效。然而，这种疾病的确切发病机制仍然是特发性的。本研究基于 Pubmed 数据库信息 (2002-2021)，使用“再生障碍性贫血”、“造血干细胞生态位”、“信号通路”、“细胞因子”和“免疫细胞”等词。在这种疾病中，造血干细胞和间充质基质细胞均受损，这与造血功能受损和造血细胞减少有关。炎性细胞因子增加，从而改变T淋巴细胞的比例并导致疾病进展。此外，AA最常见的机制是免疫系统的损害，从而导致祖细胞凋亡增加。我们在这篇综述中表明，该疾病涉及干细胞数量的数量缺陷和这些细胞功能的质量异常，并且许多不同细胞和分子因子的活性可以在该疾病中损害造血细胞和这些细胞的保护性底物。