In vivo studies reveal that mitochondrial Complex I deficiencies induce iron misregulation and liver iron overload that may contribute to neurodegeneration in mitochondrial disease mice, and that iron restriction is effective in reducing disease progression.

Hyperphosphatemia, by itself and in the context of chronic kidney disease, contributes to iron restrictive anemia by directly targeting the liver and elevating proinflammatory cytokines and hepcidin, which contributes to widespread tissue injury, such as skeletal muscle wasting.

A decline in iron-recycling functions of the splenic red pulp macrophages early during aging is driven by iron loading and involves their damage and a loss in red blood cell clearance capacity.

Under systemic iron overload, translational derepression of ferroportin mRNA via the IRE/IRP system antagonizes hepcidin-mediated ferroportin degradation to coordinately control serum iron.

An unbiased genome-wide human forward genetic screen identifies the vacuolar ATPase complex and assembly factors as regulators of HIF stability through their actions on intracellular iron metabolism.

NCOA4, the ferritin autophagy receptor, is regulated by HERC2 in an iron-dependent manner and is critical for red blood cell development.

Transferrin receptor 1-mediated iron uptake plays a pivotal role in osteoclast energy metabolism and cytoskeleton and regulates bone remodeling in female mice.

Myoglobin iron contributes to the formation and poor healing of muscle pressure injuries, that is, bedsores, and iron-chelation therapy can be administered after prolonged pressure to increase survival of the damaged tissue.

The intestine contains distinct subregions specialized for digestion along its anterior-posterior axis, and the stem cells that constantly renew these subregions are not interchangeable.

Post-menopausal women with atherosclerosis need to take the correct timing for hormone replacement therapy.