Evidence map›Paper›PMID 40684422›Full record

ArticleNeuroscience bulletin2026

Single-Cell Sequencing Reveals Circadian Sensitivity of Noise-Induced Hearing Loss Mediated by Macrophage-Driven NLRP3 Inflammasome Activation.

Qingping Ma, Qixuan Wang, Zixuan Zhu, Qian Zhou, Zhongying Wang, Minfei Qian, Teng Li, Xixi Gu, Zechuan Chen, Xueling Wang and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neuroscience bulletin, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors.

Qingping Ma *Department of Otolaryngology-Head and Neck Surgery, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200011, China.
Qixuan Wang *Department of Facial Plastic and Reconstructive Surgery, Eye & ENT Hospital of Fudan University, ENT Institute, Eye & ENT Hospital of Fudan University, NHC Key Laboratory of Hearing Medicine, Fudan University, Shanghai, 200031, China.
Zixuan Zhu *National Key Laboratory of Immune Response and Immunotherapy, Shanghai Institute of Immunity and Infection, Chinese Academy of Sciences, Shanghai, 200031, China.
Qian ZhouDepartment of Otolaryngology-Head and Neck Surgery, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200011, China.
Zhongying WangDepartment of Otolaryngology-Head and Neck Surgery, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200011, China.
Minfei QianDepartment of Otolaryngology-Head and Neck Surgery, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, China.
Teng LiNational Key Laboratory of Immune Response and Immunotherapy, Shanghai Institute of Immunity and Infection, Chinese Academy of Sciences, Shanghai, 200031, China.
Xixi GuNational Key Laboratory of Immune Response and Immunotherapy, Shanghai Institute of Immunity and Infection, Chinese Academy of Sciences, Shanghai, 200031, China.
Zechuan ChenNational Key Laboratory of Immune Response and Immunotherapy, Shanghai Institute of Immunity and Infection, Chinese Academy of Sciences, Shanghai, 200031, China.
Xueling WangDepartment of Otolaryngology-Head and Neck Surgery, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200011, China. xuelingwang2013@163.com.
Xiaoming ZhangNational Key Laboratory of Immune Response and Immunotherapy, Shanghai Institute of Immunity and Infection, Chinese Academy of Sciences, Shanghai, 200031, China. xmzhang@ips.ac.cn.
Zhiwu HuangDepartment of Otolaryngology-Head and Neck Surgery, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200011, China. huangzw86@126.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Circadian sensitivity significantly influences the severity of noise-induced hearing loss (NIHL), but the underlying mechanisms remain unclear. Here, we applied single-cell RNA sequencing to 97,043 cochlear cells, identifying macrophages as the primary immune responders to acoustic trauma, with a notable increase in their proportion in the cochlea. Immunofluorescence confirmed significant recruitment and activation of cochlear macrophages following noise exposure, while in vivo macrophage depletion resulted in the recovery of hearing. Furthermore, analyses of differentially-expressed genes and pathways revealed pronounced activation of NLRP3 inflammasome signaling in macrophages during night-time noise exposure. Measurements of elevated IL-1β and IL-18 expression in cochlear macrophages by multiplex immunohistochemistry correlated with heightened inflammation in the night-time exposure group. These findings were further confirmed by the administration of the selective NLRP3 inhibitor CY-09, which mitigated inflammasome activation, preserved synaptic integrity, and protect against hearing loss. In conclusion, our findings underscore the role of macrophage-driven NLRP3 inflammasome activation in mediating circadian variations in cochlear damage, offering a potential therapeutic target for mitigating NIHL.

Indexed as

Circadian RhythmHearing Loss, Noise-InducedInflammasomesMacrophagesNLR Family, Pyrin Domain-Containing 3 ProteinAnimalsCochleaMaleMiceMice, Inbred C57BLSingle-Cell AnalysisInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseCircadian rhythmMacrophageNLRP3 inflammasomeNoise-induced hearing loss

Identifiers

PMID40684422
PMCPMC12876505

What OpenQuestion holds

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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.