老化与每个研究组织的突变负担增加有关。间歇性地，健康增强的突变会出现，导致干细胞克隆扩张。这个过程在多个组织中都会发生，但在血液中被最好地研究了。克隆性造血性疾病与血液癌症的风险增加有关，例如急性髓系白血病，如果发生额外的配合突变，就会导致这种情况发生。令人惊讶的是，它还与非恶性疾病的风险增加有关，例如动脉粥样硬化性心血管疾病。这可能是由于变异的固有免疫细胞中增强的炎症，临床上可以用抗炎药物来针对它。最近的研究发现了其他预测克隆造血性疾病患者不良预后的因素，如突变克隆的大小、突变驱动基因和表观老化。尽管克隆性是不可避免的，而且很大程度上是时间函数，但最近的研究表明，遗传基因的遗传差异也可以影响这个过程。克隆性造血提供了一个理解年龄相关的组织干细胞成分和功能如何影响人类健康的范例。

Aging is associated with increased mutational burden in every tissue studied. Occasionally, fitness-increasing mutations will arise, leading to stem cell clonal expansion. This process occurs in several tissues but has been best studied in blood. Clonal hematopoiesis is associated with an increased risk of blood cancers, such as acute myeloid leukemia, which result if additional cooperating mutations occur. Surprisingly, it is also associated with an increased risk of nonmalignant diseases, such as atherosclerotic cardiovascular disease. This may be due to enhanced inflammation in mutated innate immune cells, which could be targeted clinically with anti-inflammatory drugs. Recent studies have uncovered other factors that predict poor outcomes in patients with clonal hematopoiesis, such as size of the mutant clone, mutated driver genes, and epigenetic aging. Though clonality is inevitable and largely a function of time, recent work has shown that inherited genetic variation can also influence this process. Clonal hematopoiesis provides a paradigm for understanding how age-related changes in tissue stem cell composition and function influence human health.