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Peer-reviewedCC BY 4.0Aging Cell

The Vicious Cycle of Sleep Disruption and Inflammaging: Mechanisms, Consequences, and Therapeutic Opportunities

  • Fu‐Ying Zhao1
  • Jia‐Mei Wang2
  • Shi‐Yang Lu1
  • Liang Hao1,3
  • Hai‐Yan Zhang4
  • Hua‐Qin Wang1
4 affiliations
  1. 1Department of Biochemistry & Molecular Biology China Medical University Shenyang Liaoning Province China
  2. 2Department of Laboratory Medicine The First Hospital of China Medical University Shenyang Liaoning Province China
  3. 3Department of Chemistry, School of Forensic Medicine China Medical University Shenyang China
  4. 4Department of Geriatrics The First Affiliated Hospital of China Medical University Shenyang Liaoning Province China
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Abstract

Aging is characterized by two interdependent hallmarks: a chronic low‐grade inflammatory state known as inflammaging, and a progressive deterioration of sleep and circadian rhythms. Emerging evidence indicates that these are not merely parallel processes but are mechanistically intertwined in a self‐perpetuating cycle. This review synthesizes current knowledge on how age‐related sleep and circadian disturbances exacerbate inflammaging through distinct molecular and cellular pathways. We examine the nocturnal dysregulation of the immune system, focusing on innate immune hyperactivation (e.g., via NLRP3 inflammasome and TLR4 signaling), cellular senescence (SASP), adaptive immune decline (T‐cell aging), and disruption of systemic pathways such as the gut‐brain axis. Clinical and epidemiological data link sleep disorders, particularly obstructive sleep apnea, to elevated inflammatory markers, accelerated epigenetic aging, and cognitive decline. Conversely, inflammaging impairs circadian regulatory structures, further degrading sleep quality. Interventions targeting the sleep‐immune axis, including melatonin, circadian reinforcement, senotherapeutics, and lifestyle modifications, hold promise for mitigating inflammaging. We conclude that sleep disruption is not a passive symptom but an active driver of immunological aging, and propose that targeting this axis represents a viable strategy for promoting healthy longevity.

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Cite

BibTeXRIS
BibTeX
@article{zhao2026vicious,
  title = {{The Vicious Cycle of Sleep Disruption and Inflammaging: Mechanisms, Consequences, and Therapeutic Opportunities}},
  author = {Fu‐Ying Zhao and Jia‐Mei Wang and Shi‐Yang Lu and Liang Hao and Hai‐Yan Zhang and Hua‐Qin Wang},
  journal = {Aging Cell},
  year = {2026},
  month = nov,
  doi = {10.1111/acel.70798},
  url = {https://doi.org/10.1111/acel.70798},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - The Vicious Cycle of Sleep Disruption and Inflammaging: Mechanisms, Consequences, and Therapeutic Opportunities
AU  - Fu‐Ying Zhao
AU  - Jia‐Mei Wang
AU  - Shi‐Yang Lu
AU  - Liang Hao
AU  - Hai‐Yan Zhang
AU  - Hua‐Qin Wang
PY  - 2026
DA  - 2026/11/04
JO  - Aging Cell
DO  - 10.1111/acel.70798
UR  - https://doi.org/10.1111/acel.70798
AB  - Aging is characterized by two interdependent hallmarks: a chronic low‐grade inflammatory state known as inflammaging, and a progressive deterioration of sleep and circadian rhythms. Emerging evidence indicates that these are not merely parallel processes but are mechanistically intertwined in a self‐perpetuating cycle. This review synthesizes current knowledge on how age‐related sleep and circadian disturbances exacerbate inflammaging through distinct molecular and cellular pathways. We examine the nocturnal dysregulation of the immune system, focusing on innate immune hyperactivation (e.g., via NLRP3 inflammasome and TLR4 signaling), cellular senescence (SASP), adaptive immune decline (T‐cell aging), and disruption of systemic pathways such as the gut‐brain axis. Clinical and epidemiological data link sleep disorders, particularly obstructive sleep apnea, to elevated inflammatory markers, accelerated epigenetic aging, and cognitive decline. Conversely, inflammaging impairs circadian regulatory structures, further degrading sleep quality. Interventions targeting the sleep‐immune axis, including melatonin, circadian reinforcement, senotherapeutics, and lifestyle modifications, hold promise for mitigating inflammaging. We conclude that sleep disruption is not a passive symptom but an active driver of immunological aging, and propose that targeting this axis represents a viable strategy for promoting healthy longevity.
SN  - 1474-9718
SN  - 1474-9726
ER  -