Hmox1/CO regulates retina regeneration via modulation of Wnt/β-catenin signalling and induction of vaspb in zebrafish

Hmox1a is rapidly induced after retinal injury in zebrafish, and Hmox1/CO signalling stabilizes β-catenin to drive vaspb expression during Muller glia reprogramming.

• Why it matters: Injury-responsive signals that trigger Muller glia stem-cell reprogramming in zebrafish are not fully defined, limiting understanding of how regeneration is initiated and sustained.
• What they did: After injury, hmox1a induction was mapped to photoreceptors and peaked during the Muller glia proliferation window; pharmacological inhibition and morpholino knockdown assessed inflammation, MGPC proliferation, and lamination, while CO delivery tested rescue and Wnt/β-catenin links.
• The result: Hmox1 loss dysregulated acute inflammation, impaired MGPC proliferation, and caused lasting lamination deficits, while exogenous CO partially rescued; mechanistically, Hmox1/CO likely represses dkk1b to stabilize β-catenin, enriching at a Tcf7l2 site to induce vaspb, with Nfe2l2a proposed as an intermediary.

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