ArticleAnimal models and experimental medicine2026
Gorab deficiency in skin dermis accelerates aging and is associated with dysregulation of RCHY1-mediated P53 ubiquitination.
Article in Animal models and experimental medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundMutations in and functional inactivation of the Gorab gene cause gerodermia osteodysplastica (GO), a disease featuring wrinkled skin and osteoporosis, but the underlying mechanisms of skin aging remain incompletely understood.
methodsBy crossing the Gorab conditional knockout mouse model (Gorab
resultsConditional knockout of Gorab at two different time points (embryonic and postnatal) resulted in elevated levels of aging-related proteins (P53, P21, P16) and a reduction in levels of extracellular matrix (ECM) components, including collagen, fibrillin-1, vimentin, fibronectin, laminin, and versican in the ventral and dorsal skin of adult mice. Postnatal knockout had a relatively more pronounced effect on skin aging-related changes. Mechanistically, Gorab knockout impaired the ubiquitination and promoted the accumulation of P53 protein, likely through regulating the E3 ligase RCHY1. This was accompanied by increased HDAC2 levels, reduced histone acetylation, and consequent downregulation of skin ECM proteins, outlining a potential pathway for accelerated skin aging.
conclusionsThis study elucidates that Gorab mutations in the dermis promote skin aging by causing P53 accumulation and disrupting ECM expression via epigenetic regulation. These findings clarify the biological role of Gorab in skin aging and provide a theoretical basis for related mechanistic research and potential preventive strategies.
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