ArticlePLoS computational biology2025
Proteostasis signatures in human diseases.
Article in PLoS computational biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Traumatic brain injury induces cell-type-specific remodelling of the proteostasis network.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026Article
- Ligand-driven modulation of chaperone-cochaperone networks shapes proteostasis outcomes.Protein science : a publication of the Protein Society · 2026Article
- Heat shock proteins (Hsp70 and Hsp90) in neurodegeneration: pathogenic roles and therapeutic potential.Frontiers in aging neuroscience · 2026Review
- Disease-disease interactions: molecular links of neurodegenerative diseases with cancer, viral infections, and type 2 diabetes.Translational neurodegeneration · 2025Review
- Cross-talk between aging resilience pathways and autoimmunity onset.Frontiers in immunology · 2025Review
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The protein homeostasis (proteostasis) network maintains the proteome in a functional state. Although this network has been comprehensively mapped, its perturbations in disease remain incompletely characterised. To address this problem, here we define the proteostasis signatures, which represent the characteristic patterns of change in the proteostasis network associated with disease. We performed a large-scale, pan-disease analysis across 32 human diseases spanning 7 disease types. We first identified unique proteostasis perturbations in specific disease states. We then uncovered distinctive signatures differentiating disease types, pointing to a range of proteostasis mechanisms in disease development. Next, we tracked the temporal evolution of proteostasis signatures, revealing shifts in proteostasis disruption over the course of disease progression. Finally, we demonstrated how smoking, a major risk factor for many diseases, impairs proteostasis in a manner similar to disease, potentially creating a predisposed environment for disease onset. These results illustrate the opportunities offered by the study of human diseases from the perspective of proteostasis signatures.
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Registered trials
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