Evidence map›Paper›PMID 42684361›Full record

ArticleNoise & health

An Oxidative Stress Biomarker for Noise-Associated Stroke: Evidence from Human and Mice.

CongCong Wu, Xiao Yu, Tian Lv, Jia Huang

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Article in Noise & health. 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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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

CongCong WuDepartment of Neurosurgery, The First People's Hospital of Yunnan Province, School of Medicine, Kunming University of Science and Technology, Kunming, China.
Xiao YuShanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, China.
Tian LvDepartment of Neurology, Zhuji Affiliated Hospital of Wenzhou Medical University, Zhuji, Zhejiang, China.
Jia HuangDepartment of Otolaryngology, Zhuji Affiliated Hospital of Wenzhou Medical University, Zhuji, Zhejiang, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundOccupational noise exposure is a recognized risk factor for stroke, yet biomarkers specific to noise-associated stroke (NAS) remain unclear. Oxidative stress (OS) plays a key mechanistic role in noise-induced cerebrovascular damage. We aim to identify OS biomarkers of NAS and conduct risk assessment.

methodsCandidate OS biomarkers were screened using Gene Expression Omnibus transcriptomic datasets integrated with eight machine-learning approaches, then verified in UK Biobank longitudinal data and in stroke model mice after 4-week noise exposure. In addition, the relationship between oxidative balance score (OBS) and stroke was evaluated among noise-exposed adults in the National Health and Nutrition Examination Survey (NHANES) 2005-2018 using logistic regression, and quartiles were applied to determine optimal cut-points.

resultsEight OS-related genes were identified, of which seven were validated in stroke mice. C-C Motif Chemokine Ligand 3 (CCL3) emerged as the key biomarker. In UK Biobank, occupational noise increased CCL3 expression (effect = 0.052, P  = 0.038), and higher CCL3 levels predicted greater stroke risk (hazard ratio = 1.15, P < 0.001). Functionally, CCL3 drove neuroinflammation via chemokine signaling. In noise-exposed stroke mice, circulating CCL3 increased ( P  = 0.014) and infarct volume enlarged by 12.9% ( P  = 0.011). Among 3306 noise-exposed NHANES participants, higher OBS was protective (odd ratio [OR] = 0.97, P  = 0.01), whereas OBS <10 markedly elevated stroke risk (OR = 2.40, P  = 0.033) compared with the OBS >24 group.

conclusionCCL3 is a validated OS biomarker linking occupational noise exposure to stroke. Maintaining OBS >18 through dietary and lifestyle strategies may mitigate NAS risk and offer a targeted neuroprotective approach for noise-exposed populations.

Indexed as

Chemokine CCL3Noise, OccupationalOccupational ExposureOxidative StressStrokeAdultAgedAnimalsBiomarkersDisease Models, AnimalFemaleHumansMaleMiceMiddle AgedRisk AssessmentBiomarkersChemokine CCL3chemokine ccl3noiseoccupational exposureoxidative stressstroke

Identifiers

PMID42684361
PMCPMC13623172

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.