Slc39a13, also known as ZIP13, is a zinc transporter that has been found to be involved in multiple crucial biological functions. It plays a role in iron transport and homeostasis, as well as in the BMP/TGF-beta signaling pathways, which are important for connective tissue development [1,5].

In gene knockout studies, Zip13-knockout male mice show iron deposition in several tissues, indicating that ZIP13 is crucial for iron homeostasis, possibly by shunting iron from the cytosol to the ER/Golgi hub [1]. Zip13-knockout mice also exhibit abnormalities in the aortic wall and cornea, such as changes in the number and morphology of elastic and cellular components in the aorta, and various morphometric differences in the cornea [2,4]. These phenotypes suggest the importance of Slc39a13 in maintaining the integrity of connective tissues. Additionally, down-regulation of ZIP13 in mouse hearts leads to activation of CaMKII at reperfusion, exacerbating myocardial ischemia/reperfusion injury [3].

In conclusion, Slc39a13 is essential for iron homeostasis and connective tissue development. The study of Slc39a13 knockout mouse models has provided insights into its role in diseases related to iron metabolism disorders, connective tissue dysfunctions like Ehlers-Danlos syndrome, and myocardial ischemia/reperfusion injury. Understanding the functions of Slc39a13 can potentially lead to new strategies for treating these diseases.