ArticleAmerican journal of translational research2026
Integrated multi-omics atlas reveals PTM-driven signaling and immunologic remodeling in a mouse model of age-related subclinical hypothyroidism.
Article in American journal of translational research, 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
objectiveAge-related subclinical hypothyroidism (AR-SCH) profoundly impairs thyroid structural and functional integrity in the elderly, yet the systemic molecular architecture driving AR-SCH pathogenesis remains poorly understood. This study aimed to construct a comprehensive multi-omic atlas of the AR-SCH mouse thyroid.
methodsGlobal proteomics, site-specific N-glycoproteomics, and phosphoproteomics were integrated to profile thyroid tissues from AR-SCH and control mice.
resultsIn total, 6,666 proteins, 2,476 site-specific N-glycans, and 11,929 phosphorylation sites were identified. Global proteomics revealed a widespread reduction of functional proteins (81.7% downregulated), primarily associated with cytoskeletal structural remodeling and tissue degeneration under AR-SCH conditions. N-glycoproteomics identified altered fucosylation and reduced N-glycosylation associated with extracellular-matrix organization and local immune-related processes. Furthermore, an extensive hypophosphorylation trend (91.53% downregulated sites) was associated with suppression of intracellular signaling cascades, possibly involving autophagic clearance and perturbed apoptotic homeostasis.
conclusionMulti-omics integration suggests an interconnected network as a convergent hallmark of AR-SCH progression, characterized by cytoskeletal reconfiguration, immune regulation shifts, and signaling attenuation that synergistically contribute to systemic thyroid decline, offering a therapeutic window for preserving endocrine homeostasis.
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