A patient with acrodermatitis enteropathica has a mutation in SLC39A4 (ZIP4), a zinc transporter. Zinc deficiency impairs wound healing primarily because zinc is a cofactor for:

• A Prolyl hydroxylase, which is required for hydroxylation of proline residues in collagen triple helix stabilisation
• B Matrix metalloproteinases (MMPs), which are zinc-dependent endopeptidases required for ECM remodelling during wound healing ✓
• C Lysyl oxidase, the copper-dependent enzyme crosslinking collagen and elastin
• D Hyaluronidase, which degrades hyaluronic acid to enable cell migration into the wound bed

Explanation

Matrix metalloproteinases (MMPs — collagenases, gelatinases, stromelysins) are zinc-metalloenzymes that require zinc at their catalytic site for endopeptidase activity. These enzymes are critical during wound healing for ECM remodelling, cell migration, angiogenesis, and scar remodelling. Zinc deficiency impairs MMP activity, disrupting wound healing. Additionally, zinc is required for numerous transcription factors (zinc finger proteins), immune function, and DNA synthesis. Prolyl hydroxylase requires iron and ascorbic acid (vitamin C), not zinc. Lysyl oxidase is copper-dependent.

Reference: Harper's Illustrated Biochemistry, 32nd ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.