Zinc transport and homeostasis

Zinc transport and homeostasis refers to the coordinated physiological processes that regulate the acquisition, distribution, and storage of zinc ions within an organism, primarily managed by the Solute Carrier (SLC) families SLC30 (ZnT) and SLC39 (ZIP) and the storage protein metallothionein (Kambe et al., 2015). Zinc is an essential trace element serving as a structural or catalytic component for over 10% of the human proteome, including enzymes like carbonic anhydrase and thousands of zinc-finger transcription factors (Bafaro et al., 2017). Dysregulation of zinc homeostasis is implicated in numerous pathologies; for instance, mutations in SLC39A4 cause the severe deficiency disorder acrodermatitis enteropathica, while SLC30A8 (ZnT8) is a major autoantigen in type 1 diabetes and a risk factor for type 2 diabetes (Wessels et al., 2017). Pharmacological intervention typically involves zinc supplementation for deficiency, chelation for toxicity, or the use of ionophores like clioquinol to redistribute zinc in neurodegenerative contexts (Bafaro et al., 2017). Because zinc is ubiquitous and involved in diverse signaling pathways, targeting specific transporters remains a significant challenge due to the risk of systemic toxicity and off-target effects on global metal ion balance (Plum et al., 2010).

Other names

Zinc homeostasisZinc metabolismZinc ion transportZIP and ZnT transport system

Zinc supplementation, Zinc chelation, Zinc ionophore-mediated redistribution, Transporter inhibition