Department of Biomedical Sciences for Health, University of Milan, 20133 Milano, Italy.
Int J Mol Sci. 2021 Mar 15;22(6):2986. doi: 10.3390/ijms22062986.
Body iron levels are regulated by hepcidin, a liver-derived peptide that exerts its function by controlling the presence of ferroportin (FPN), the sole cellular iron exporter, on the cell surface. Hepcidin binding leads to FPN internalization and degradation, thereby inhibiting iron release, in particular from iron-absorbing duodenal cells and macrophages involved in iron recycling. Disruption in this regulatory mechanism results in a variety of disorders associated with iron-deficiency or overload. In recent years, increasing evidence has emerged to indicate that, in addition to its role in systemic iron metabolism, FPN may play an important function in local iron control, such that its dysregulation may lead to tissue damage despite unaltered systemic iron homeostasis. In this review, we focus on recent discoveries to discuss the role of FPN-mediated iron export in the microenvironment under both physiological and pathological conditions.
体内铁水平受铁调素调控，铁调素是一种由肝脏产生的肽，通过控制位于细胞表面的唯一的细胞铁输出蛋白（ ferroportin ，FPN）的存在来发挥作用。铁调素与 FPN 结合导致 FPN 内化和降解，从而抑制铁的释放，特别是从铁吸收的十二指肠细胞和参与铁循环的巨噬细胞中释放铁。这种调节机制的破坏会导致各种与缺铁或铁过载相关的疾病。近年来，越来越多的证据表明，除了在全身铁代谢中的作用外，FPN 可能在局部铁控制中发挥重要作用，因此尽管系统铁稳态没有改变，但其失调也可能导致组织损伤。在这篇综述中，我们将重点讨论最近的发现，以讨论在生理和病理条件下，FPN 介导的铁输出在微环境中的作用。
