GALNT3 in Ischemia-Reperfusion Injury of the Kidney

What is it about?

Damages to subcellular organelles, such as mitochondria and endoplasmic reticulum, are well-recognized in tubular cell injury and death in acute kidney injury (AKI). However, the changes and involvement of Golgi apparatus are much less known. Here, we report the regulation and role of N-acetylgalactosaminyltransferase-3 (GALNT3), a key enzyme for protein glycosylation in Golgi apparatus, in AKI. Functionally, blockage of GALNT3 either by gene silence in cells or pharmacologic inhibition in mice exacerbated ischemic AKI, supporting a protective role of GALNT3 in AKI. Further mechanistic investigations suggest that GALNT3 might contribute to epidermal growth factor receptor (EGFR) signaling by O-glycosylation of EGFR. Together, these results indicate that GALNT3 may protect kidney tubular cells in AKI by mediating EGFR signaling.

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