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Cdc42 and aging of hematopoietic stem cells

机译：Cdc42与造血干细胞的衰老

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Purpose of Review: Hematopoietic stem cells (HSCs) continuously provide mature blood cells during the lifespan of a mammal. The functional decline in hematopoiesis in the elderly, which involves a progressive reduction in the immune response and an increased incidence of myeloid malignancy, is partly linked to HSC aging. Molecular mechanisms of HSC aging remain unclear, hindering rational approaches to slow or reverse the decline of HSC function with age. Identifying conditions under which aged HSCs become equivalent to young stem cells might result in treatments for age-associated imbalances in lymphopoiesis and myelopoiesis and in blood regeneration. RECENT FINDINGS: Aging of HSCs has been for a long time thought to be an irreversible process imprinted in stem cells due to the intrinsic nature of HSC aging. Mouse model studies have found that aging is associated with elevated activity of the Rho GTPase Cdc42 in HSCs that is causative for loss of polarity, altered epigenetic modifications and functional deficits of aged HSCs. The work suggests that inhibition of Cdc42 activity in aged HSCs may reverse a number of phenotypes associated with HSC aging. SUMMARY: Maintaining the regenerative capacity of organs or organ systems may be a useful way to ensure healthy aging. A defined set of features phenotypically separate young from aged HSCs. Aging of HSCs has been thought to be irreversible. Recent findings support the hypothesis that functional decline of aged HSCs may be reversible by pharmacological intervention of age altered signaling pathways and epigenetic modifications.
机译：审查目的：造血干细胞（HSC）在哺乳动物的生命周期中不断提供成熟的血细胞。老年人造血功能的下降，包括免疫反应的逐步降低和髓系恶性肿瘤的发生率增加，部分与HSC衰老有关。 HSC衰老的分子机制仍不清楚，阻碍了合理的方法来减缓或逆转HSC功能随年龄的下降。确定老年HSC与年轻干细胞相当的条件可能会导致与年龄相关的淋巴细胞生成和骨髓生成失衡以及血液再生的治疗。最近的发现：由于HSC衰老的内在本质，长期以来，HSC的衰老一直被认为是在干细胞中不可逆转的过程。小鼠模型研究发现，衰老与HSC中Rho GTPase Cdc42的活性升高有关，这是导致衰老的HSC极性丧失，表观遗传修饰改变和功能缺陷的原因。这项工作表明，在衰老的HSC中抑制Cdc42活性可能会逆转许多与HSC衰老相关的表型。摘要：维持器官或器官系统的再生能力可能是确保健康衰老的有用方法。一组明确的特征在表型上将年轻人与老年HSC分开。人们认为，HSC的老化是不可逆的。最新发现支持以下假设，即年龄变化的信号通路和表观遗传修饰的药理干预可逆转老年HSC的功能下降。

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