Slc39a7, also known as ZIP7, is an intracellular zinc transporter. It plays important roles in various biological processes by regulating zinc homeostasis. It is involved in pathways such as TNF-α-mediated NF-κB signaling, TGF-β/SMAD pathway, and Akt/mTOR signaling pathway, and is crucial for maintaining normal cell functions and tissue integrity [2,4,5].

In the context of intervertebral disc degeneration, NLRX1 forms a complex with Slc39a7 on the mitochondrial membrane of nucleus pulposus cells, modulating mitochondrial Zn2+ trafficking and orchestrating mitochondrial dynamics and mitophagy, which is beneficial for maintaining intervertebral disc integrity [1].

In myocardial reperfusion injury, cardiac-specific ZIP7 conditional knockout (ZIP7 cKO) mice studies showed that KO or cKO of ZIP7 increased mitophagy under physiological conditions, and ZIP7 cKO reduced mitochondrial ROS generation and myocardial infarction via a PINK1-dependet manner, indicating that ZIP7 upregulation leading to suppression of mitophagy is a critical feature of myocardial reperfusion injury [3].

In cancer research, knockdown of Slc39A7 in cervical and colorectal cancer cells inhibited cell proliferation, induced apoptosis, and attenuated migratory and invasive ability, suggesting its role in cancer progression [6,7].

In conclusion, Slc39a7 is essential for regulating zinc-related biological functions and is involved in multiple disease processes, including intervertebral disc degeneration, myocardial reperfusion injury, and cancer. Gene knockout or conditional knockout mouse models have been instrumental in revealing its functions in these specific disease areas, providing potential therapeutic targets for related diseases.