Stress-response enzyme helps zebrafish repair their retinas
Blocking the enzyme impaired retinal recovery in zebrafish experiments, while carbon monoxide, one of its products, partly rescued the defects.

Our read
Mechanisms- Studied:
- Preprint: experiments in zebrafish with injured retinas
- What changed:
- Blocking Hmox1 activity or reducing its production left lasting defects in retinal layers in injured zebrafish
- The catch:
- Reported recovery outcomes covered retinal structure and cell division, but not visual function
- In the record:
- One of 76 papers on carbon monoxide on record: 23 with results in people, 2 in animals.
- Why it’s aging research:
- Repairing, replacing or regenerating the aging body.
Editor of record: Boris Djordjevic · AgingResearch.News
In zebrafish with injured retinas—the eye’s light-sensing tissue—researchers tested Hmox1, an enzyme activated by stress, in animal experiments. They blocked its activity with a drug or reduced its production with a gene-targeting technique. These interventions disrupted the early inflammatory response, reduced division of immature cells derived from Müller glia, the retina’s support cells, and left lasting defects in the arrangement of retinal layers.
Carbon monoxide, a product of Hmox1 activity, partly rescued each of these effects. The authors proposed that Hmox1 and carbon monoxide act through a chain of signals involving Wnt, a cell communication system, to help Müller glia take on a stem-cell-like role.
Why it matters
Müller glia retain a capacity to act as stem cells in zebrafish that mammals lack. The authors identified Hmox1 and carbon monoxide as candidate targets for investigating retinal regeneration in mammals.
Caveats
The experiments tested recovery from retinal injury in zebrafish, not people, and the proposed signaling chain remains tentative. The work is a preprint and has not been peer-reviewed.
- Carbon monoxide
- hmox1a
- Inflammation
- HMOX1A expression
- Müller glia-derived progenitor cell proliferation
- Zebrafish
The paper
S. N. Pradhan Centre for Neurosciences, University of Calcutta, India
bioRxiv, Nov 3, 2026, Open access, CC BY-NC-ND, Preprint, not yet peer-reviewed
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