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Dormant Vitamin A Gene Switch Restores Ear Regeneration in Mice

Scientists revealed that boosting retinoic acid signaling through genetic activation of Aldh1a2 can reverse evolutionary suppression of tissue regrowth

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Gloved hands of laboratory technician injecting mouse held in petri dish with clear liquid from syringe. Mouse resting calmly in controlled lab environment maintained for research
A tiny European Wood Mouse eating the nuts and seeds in the bowl of a garden figurine.
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Overview

  • Comparative single-cell RNA sequencing and spatial transcriptomics showed that regenerative mammals activate Aldh1a2 in wound-induced fibroblasts while mice exhibit deficient expression and faster retinoic acid breakdown.
  • Exogenous retinoic acid injections or insertion of a rabbit-derived Aldh1a2 enhancer fully restored closure of full-thickness ear pinna injuries in genetically modified mice.
  • Aldh1a2 encodes an enzyme critical for synthesizing retinoic acid, a metabolite that reawakens embryonic-like pathways for cell proliferation, migration and tissue patterning.
  • Analysis suggests that evolutionary loss of Aldh1a2-linked regulatory elements contributed to the limited regenerative capacity observed in common rodent species.
  • Published in Science on June 26, 2025, the study opens avenues for gene therapy and pharmacological approaches aimed at enhancing human tissue repair and regeneration.