Core Insights - The research identifies Aldh1a2 gene expression deficiency as a key factor in the failure of ear regeneration in mice, while activation of this gene allows for successful regeneration [1][3] - The study highlights the differences in gene regulation between rabbits and mice, with rabbits retaining critical DNA sequences that activate Aldh1a2, leading to effective tissue regeneration [3] - The findings suggest potential applications in regenerative medicine, offering new strategies for organ regeneration, including complex organs like the brain and heart [3] Group 1 - The research team from Beijing Huada Life Science Research Institute and Beijing Institute of Life Sciences used rabbit and mouse ear models to study regeneration capabilities [1] - Rabbits can repair ear hole injuries of 4mm to 8mm within a month, while mice lack this ability [1] - The study utilized single-cell sequencing and spatiotemporal omics to analyze the high-resolution dynamics of ear regeneration and healing processes [1] Group 2 - Insufficient synthesis of retinoic acid, a metabolite of vitamin A crucial for cell development, is linked to the failure of ear regeneration in mice [3] - The research indicates that activating Aldh1a2 or supplementing with retinoic acid can lead to the emergence of pluripotent cells in adult mice, enabling the reconstruction of ear cartilage and nerve tissue [3] - The implications of this research extend beyond ear regeneration, potentially advancing regenerative medicine from basic research to clinical applications [3]