ArticleInternational journal of molecular sciences2026
Proteome-Level Autophagy-Lysosome Remodelling Marks Ageing in Human Dermal Fibroblasts and Nominates Hydroxytyrosol as a Candidate Nutraceutical.
Article in International journal of molecular sciences, 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
Autophagy-lysosome dysfunction accompanies dermal fibroblast ageing, yet whether remodelling is transcriptional or post-transcriptional in primary human cells remains unresolved. We reanalysed the Genetic and Epigenetic Signatures of Translational Ageing Laboratory Testing(GESTALT) paired RNA sequencing (RNA-seq) and tandem mass tag (TMT) proteome from 82 donors (aged 22-89) using Data Integration Analysis for Biomarker discovery using Latent cOmponents (DIABLO) for supervised multi-omics integration, weighted gene co-expression network analysis (WGCNA), external Genotype-Tissue Expression(GTEx) transcriptomic comparison, network medicine proximity mapping and CDOCKER molecular docking. Three analyses converged on the autophagy-lysosome axis: Kyoto Encyclopaedia of Genes and Genomes (KEGG) Lysosome ranked first in discordant-quadrant analysis; gene set enrichment analysis (GSEA) identified vacuole organisation and macroautophagy as the top age-upregulated Gene Ontology (GO) terms; and WGCNA recovered KEGG Lysosome in the brown module. Module regression localised most proteomic age signals to the lysosomal degradative-capacity module, whereas the proteasome was unaffected. McNemar testing and GTEx comparison supported a protein-side, post-transcriptional origin. TCIRG1, CTSA and ATP6V0D1 were recurrent hubs. Network proximity computationally prioritised hydroxytyrosol as a lysosomal-degradative-capacity-preferential candidate, and CDOCKER on cathepsin A linked its advantage over tyrosol to an ortho-hydroxyl group forming additional hydrogen bonds. These results support protein-layer-dominant autophagy-lysosome remodelling as a feature of dermal fibroblast ageing and suggest a cell-type-resolved computational route from ageing proteomics to testable dietary candidates.
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