Evidence map›Paper›PMID 32026209›Full record

ArticleBiogerontology2020

D-Galactose-induced oxidative stress and mitochondrial dysfunction in the cochlear basilar membrane: an in vitro aging model.

Bin Guo, Qing Guo, Zhan Wang, Jian-Bo Shao, Ke Liu, Zheng-De Du, Shu-Sheng Gong

Open access · hybridAbstract read
In one paragraph

Article in Biogerontology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.7field-weighted citation impact, top 8% of its field
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

38 citing papers in PubMed, 70 citations in OpenAlex.

  1. Review
  2. Vitamin D Promotes Neuronal Survival via Nrf2 Upregulation in D-Galactose-Induced Mice: An In-Vivo and In-Silico Study.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026
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  15. An Update on Neuroaging on Earth and in Spaceflight.International journal of molecular sciences · 2025
    Review
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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

7 authors at 3 institutions in 1 country.

Bin GuoDepartment of Otorhinolaryngology, Beijing Friendship Hospital, Capital Medical University, 95 Yongan Road, Xicheng District, Beijing, 100050, China.
Qing GuoDepartment of Otorhinolaryngology, Yidu Central Hospital, 4138 Linglong Shan South Road, Qingzhou, 262500, China.
Zhan WangDepartment of Biomedical Engineering, Tsinghua University, Shuangqing Road, Haidian District, Beijing, 100084, China.
Jian-Bo ShaoDepartment of Otorhinolaryngology, Beijing Children's Hospital, Capital Medical University, 56 Nanlishi Road, Xicheng District, Beijing, 100045, China.
Ke LiuDepartment of Otorhinolaryngology, Beijing Friendship Hospital, Capital Medical University, 95 Yongan Road, Xicheng District, Beijing, 100050, China.
Zheng-De DuDepartment of Otorhinolaryngology, Beijing Friendship Hospital, Capital Medical University, 95 Yongan Road, Xicheng District, Beijing, 100050, China. duzhengde@163.com.
Shu-Sheng GongDepartment of Otorhinolaryngology, Beijing Friendship Hospital, Capital Medical University, 95 Yongan Road, Xicheng District, Beijing, 100050, China. gongss@ccmu.edu.cn.ORCID 0000-0001-7885-7731
Capital Medical University · CNTsinghua University · CNYidu Central Hospital of Weifang · CN

Funding

National Natural Science Foundation of China 81700917National Natural Science Foundation of China 81771016National Natural Science Foundation of China 81830030Postdoctoral Research Foundation of China 2018M630180
6 · The paper itself

Abstract

The cochlear basilar membrane (CBM) contains inner hair cells and outer hair cells that convert sound waves into electrical signals and transmit them to the central auditory system. Cochlear aging, the primary reason of age-related hearing loss, can reduce the signal transmission capacity. There is no ideal in vitro aging model of the CBM. In this study, we cultured the CBM, which was dissected from the cochlea of the C57BL/6 mice 5 days after birth, in a medium containing 20 mg/mL, 40 mg/mL, or 60 mg/mL D-galactose (D-gal). Compared with the control group, the levels of senescence-associated β-galactosidase were increased in a concentration-dependent manner in the CBM of the D-gal groups. In addition, levels of the mitochondrial superoxide and patterns of an age-related mitochondrial DNA3860-bp deletion were significantly increased. The ATP levels and the membrane potential of the mitochondrial were significantly decreased in the CBM of the D-gal groups compared with the control group. Furthermore, in comparison with the control group, damaged hair cell stereocilia and a loss of inner hair cell ribbon synapses were observed in the CBM of the D-gal groups. A loss of hair cells and activation of caspase-3-mediated outer hair cell apoptosis were also observed in the CBM of the high-dose D-gal group. These insults induced by D-gal in the CBM in vitro were similar to the ones that occur in cochlear natural aging in vivo. Thus, we believe that this is a successful in vitro aging model using cultured CBM. These results demonstrate the effects of mitochondrial oxidative damage on presbycusis and provide a reliable aging model to study the mechanisms of presbycusis in vitro.

Indexed as

Basilar MembraneGalactoseAnimalsCochleaDNA, MitochondrialMiceMice, Inbred C57BLMitochondriaOxidative StressRatsRats, Sprague-DawleyDNA, MitochondrialGalactoseAging modelApoptosisCochlear basilar membraneD-galactoseMitochondrial oxidative damagePresbycusis

Identifiers

PMID32026209
PMCPMC7196095
OpenAlexW3005417942

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.