Ferroportin1 deficiency in mouse macrophages impairs iron homeostasis and inflammatory responses.

@article{Zhang2011Ferroportin1DI,
  title={Ferroportin1 deficiency in mouse macrophages impairs iron homeostasis and inflammatory responses.},
  author={Zhuzhen Zhang and Fan Zhang and Peng-Cheng An and Xin Guo and Yuanyuan Shen and Yunlong Tao and Qian Wu and Yuchao Zhang and Yu Yu and Bo Ning and Guangjun Nie and Mitchell D Knutson and Gregory J. Anderson and Fudi Wang},
  journal={Blood},
  year={2011},
  volume={118 7},
  pages={
          1912-22
        }
}
Systemic iron requirements are met predominantly through the recycling of iron from senescent erythrocytes by macrophages, a process in which the iron exporter ferroportin (Fpn1) is considered to be essential. Yet the role of Fpn1 in macrophage iron recycling and whether it influences innate immune responses are poorly understood in vivo. We inactivated Fpn1 in macrophages by crossing Fpn1-floxed animals with macrophage-targeted LysM-Cre or F4/80-Cre transgenic mice. Macrophage Fpn1 deletion… 
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Ferroportin1 in hepatocytes and macrophages is required for the efficient mobilization of body iron stores in mice
TLDR
Fpn1 is critical for both hepatocyte iron mobilization and macrophage iron recycling during conditions of dietary iron deficiency, revealing new insights into the relationships between Fpn1‐mediated iron mobilization, iron storage, and intestinal iron absorption and how these processes interact to maintain systemic iron homeostasis.
Ferroportin deficiency in erythroid cells causes serum iron deficiency and promotes hemolysis due to oxidative stress.
TLDR
The results indicate that FPN of erythroid cells plays an unexpectedly essential role in maintaining systemic iron homeostasis and protecting RBCs from oxidative stress, providing insight into the pathophysiology of FPN diseases.
Impaired iron recycling from erythrocytes is an early iron-dependent hallmark of aging
TLDR
RPM dysfunction is identified as an early hallmark of physiological aging and dietary iron reduction improves iron turnover efficacy and it is found that feeding mice an iron-reduced diet alleviates iron accumulation and reactive oxygen species build-up in RPMs, restores mitochondrial and lysosomal functions, and improves their ability to clear erythrocytes.
Macrophage ferroportin is essential for stromal cell proliferation in wound healing
TLDR
It is revealed that iron/ferroportin plays a largely underestimated role in macrophage trophic function in skin homeostasis and repair, a complex process leading to major clinical problems, if impaired.
Physiological functions of ferroportin in the regulation of renal iron recycling and ischemic acute kidney injury.
TLDR
FPN deletion in the proximal tubules alleviated ischemic acute kidney injury, possibly by upregulating FTH1 to limit catalytic iron and by priming antioxidant mechanisms, indicating that FPN could be deleterious in the pathophysiology of isChemic acute kidneys injury (AKI) and thus may be a potential target for the prevention and mitigation of ischymic AKI.
Characterization of ferroptosis in murine models of hemochromatosis
TLDR
Results provide compelling evidence that iron plays a key role in triggering Slc7a11‐mediated ferroPTosis and suggest that ferroptosis may be a promising target for treating hemochromatosis‐related tissue damage.
Hepatic Transferrin Plays a Role in Systemic Iron Homeostasis and Liver Ferroptosis.
TLDR
Treating hepatocyte-specific Trf knockout mice with the ferroptosis inhibitor ferrostatin-1 potently rescued liver fibrosis induced by either high dietary iron or carbon tetrachloride (CCl4) injections, and deleting hepatic Slc39a14 expression in Trf-LKO mice significantly reduced hepatic iron accumulation, indicate that hepatic transferrin plays a protective role in maintaining liver function.
Iron levels in polarized macrophages: regulation of immunity and autoimmunity.
Deletion of ferroportin in murine myeloid cells increases iron accumulation and stimulates osteoclastogenesis in vitro and in vivo
TLDR
It is indicated that FPN-regulated intracellular iron levels are critical for mitochondrial metabolism, osteoclastogenesis, and skeletal homeostasis in mice.
Iron Regulatory Proteins Mediate Host Resistance to Salmonella Infection.
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