Ganz Tomas, Nemeth Elizabeta
Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA, USA.
Semin Hematol. 2009 Oct;46(4):387-93. doi: 10.1053/j.seminhematol.2009.06.001.
Anemia of chronic disease, also called anemia of inflammation, is characterized by hypoferremia due to iron sequestration that eventually results in iron-restricted erythropoiesis. During the last decade, the molecular mechanisms of iron sequestration have been found to center on cytokine-stimulated overproduction of the iron-regulatory hormone hepcidin. The inflammatory cytokine interleukin-6 (IL-6) is a particularly prominent inducer of hepcidin, but other cytokines are likely to contribute as well. Hepcidin excess causes the endocytosis and proteolysis of the sole known cellular iron exporter, ferroportin, trapping iron in macrophages and iron-absorbing enterocytes. The supply of iron to hemoglobin synthesis becomes limiting, eventually resulting in anemia. Depending on the details of the underlying disease, other inflammation-related mechanisms may also contribute to anemia.
慢性病贫血，也称为炎症性贫血，其特征是由于铁螯合导致低铁血症，最终导致铁限制的红细胞生成。在过去十年中，已发现铁螯合的分子机制主要围绕细胞因子刺激铁调节激素铁调素的过量产生。炎性细胞因子白细胞介素-6（IL-6）是铁调素的一个特别突出的诱导剂，但其他细胞因子可能也有作用。铁调素过量导致唯一已知的细胞铁输出蛋白铁转运蛋白的内吞作用和蛋白水解，将铁捕获在巨噬细胞和吸收铁的肠细胞中。用于血红蛋白合成的铁供应变得受限，最终导致贫血。根据潜在疾病的具体情况，其他与炎症相关的机制也可能导致贫血。
