Evidence map›Paper›PMID 40018883›Full record

ArticleAging cell2025

Transforming Growth Factor-β-Activated Protein 1 (TAK1) Regulates Necroptosis in Age-Related Hearing Loss.

Hanjing Wang, Yayun Lv, He Zhao, Zhihong Hao, Xiaoyu Zhai, Yan Wang, Jingjing Qiu, Liang Chen, Jiamin Zhou, Limei Cui and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Aging cell, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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

11 authors.

Hanjing WangSchool of Clinical Medicine, Shandong Second Medical University, Weifang, Shandong, People's Republic of China.
Yayun LvDepartment of Otorhinolaryngology, Head and Neck Surgery, Yantai Yuhuangding Hospital, Qingdao University, Yantai, Shandong, People's Republic of China.
He ZhaoDepartment of Otorhinolaryngology, Head and Neck Surgery, Yantai Yuhuangding Hospital, Qingdao University, Yantai, Shandong, People's Republic of China.
Zhihong HaoSchool of Clinical Medicine, Shandong Second Medical University, Weifang, Shandong, People's Republic of China.
Xiaoyu ZhaiDepartment of Otorhinolaryngology, Head and Neck Surgery, Yantai Yuhuangding Hospital, Qingdao University, Yantai, Shandong, People's Republic of China.
Yan WangDepartment of Otorhinolaryngology, Head and Neck Surgery, Yantai Yuhuangding Hospital, Qingdao University, Yantai, Shandong, People's Republic of China.
Jingjing QiuDepartment of Otorhinolaryngology, Head and Neck Surgery, Yantai Yuhuangding Hospital, Qingdao University, Yantai, Shandong, People's Republic of China.
Liang ChenDepartment of Otorhinolaryngology, Head and Neck Surgery, Yantai Yuhuangding Hospital, Qingdao University, Yantai, Shandong, People's Republic of China.
Jiamin ZhouDepartment of Otorhinolaryngology, Head and Neck Surgery, Yantai Yuhuangding Hospital, Qingdao University, Yantai, Shandong, People's Republic of China.ORCID 0000-0002-1124-9608
Limei CuiDepartment of Otorhinolaryngology, Head and Neck Surgery, Yantai Yuhuangding Hospital, Qingdao University, Yantai, Shandong, People's Republic of China.
Yan SunDepartment of Otorhinolaryngology, Head and Neck Surgery, Yantai Yuhuangding Hospital, Qingdao University, Yantai, Shandong, People's Republic of China.ORCID 0000-0003-3384-101X

Funding

National Natural Science Foundation of China 82371153Natural Science Foundation of Shandong Province ZR2021MH378;ZR2022QH073Yantai Science and Technology Innovation Development Project 2023YD050
6 · The paper itself

Abstract

Inflammation plays an important role in age-related hearing loss (ARHL). Transforming growth factor-β-activated protein 1 (TAK1), a key factor upstream of inflammatory pathways, mediates various cell death pathways, potentially influencing the survival and death of cochlear hair cells. The DBA/2 J mouse model and the HEI-OC1 cell line were used to investigate the mechanism of TAK1-mediated inflammation in ARHL. Hematoxylin and eosin staining revealed significant histological damage in the cochlea of 16-week-old mice, along with an increase in auditory-evoked brainstem response thresholds. Concurrently, TAK1 mRNA levels decreased sharply, and necroptosis significantly increased in 16-week-old mice, indicating a correlation between TAK1 expression, necroptosis, and hearing loss. We subsequently constructed TAK1 knockdown and overexpression HEI-OC1 cells for further investigation. TAK1 knockdown in HEI-OC1 cells significantly activated the necroptotic pathway, characterized by an increase in necroptosis, along with up-regulation of RIPK3 and MLKL, and down-regulation of NF-κB and Caspase 8. However, TAK1 overexpression successfully prevented necroptosis in HEI-OC1 cells, leading to decreases in NF-κB, Caspase 8, RIPK3, and MLKL. We further treated TAK1 knockdown cells with necroptosis inhibitors and found that they could reverse the damage caused by TAK1 knockdown in HEI-OC1 cells. This preliminary study shows that TAK1-mediated necroptotic pathways play an important role in the pathogenesis of ARHL.

Indexed as

Hearing LossMAP Kinase Kinase KinasesNecroptosisAnimalsCell LineMAP Kinase Kinase Kinase 7MiceMAP Kinase Kinase Kinase 7MAP Kinase Kinase Kinasesage‐related hearing lossinflammationnecroptosispresbycusisTAK1

Identifiers

PMID40018883
PMCPMC12151908

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 Socratic graph.