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HSF1-mediated Proteostasis Decline Links Aging and Sleep Disruption
Biorxiv : the Preprint Server for Biology
|May 4, 2026
Summary
Chronic sleep disruption accelerates aging by impairing proteostasis, particularly the heat shock factor 1 (HSF1) network. This age-related decline in protein maintenance increases vulnerability to neurodegenerative diseases like Alzheimer's.
Area of Science:
- Molecular Biology
- Neuroscience
- Gerontology
Background:
- Sleep disruption is common in aging and linked to negative outcomes, but molecular links are unknown.
- Proteostasis, or protein balance, is crucial for cellular health and declines with age.
Purpose of the Study:
- To identify molecular pathways linking aging and sleep disruption.
- To investigate the role of proteostasis and heat shock factor 1 (HSF1) in this relationship.
Main Methods:
- Integrative analysis of human and mouse transcriptomic and proteomic data.
- Examined gene expression in human prefrontal cortex and peripheral blood.
- Assessed proteostasis pathways in aging mouse tissues and cell types.
Main Results:
- Proteostasis pathways, especially heat shock response, show age-associated downregulation correlating with chronic sleep disruption.
- HSF1-mediated proteostasis exhibits diminished inducibility with age and insufficient sleep, particularly in neurons.
- Vulnerability is mapped to hippocampal circuits and cortical neurons in Alzheimer's disease.
Conclusions:
- Repeated sleep disruption progressively impairs proteostatic capacity, accelerating aging and proteome maintenance decline.
- HSF1-mediated proteostasis acts as a key link between sleep stability and molecular aging.
- Sleep disruption and proteostasis decline reciprocally worsen each other, increasing aging vulnerability.
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