Evidence map›Paper›PMID 40186313›Full record

ArticleActa neuropathologica communications2025

TRPA1 exacerbates selective retinal ganglion cell vulnerability under acute ocular hypertension.

Wenhan Lu, Yu Wang, Wei Hu, Xinyi Lin, Xiaoyu Tong, Yi Tian, Yuning Chen, Yicong Wang, Yan Xiao, Hongfang Yang and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Acta neuropathologica communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Wenhan LuDepartment of Ophthalmology & Visual Science, Eye & ENT Hospital, Shanghai Medical College, Fudan University, Shanghai, 200031, China.
Yu WangDepartment of Integrative Medicine and Neurobiology, School of Basic Medical Sciences, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Fudan University, Shanghai, 200032, China.
Wei HuDepartment of Integrative Medicine and Neurobiology, School of Basic Medical Sciences, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Fudan University, Shanghai, 200032, China.
Xinyi LinDepartment of Oncology, Shanghai Medical College, Fudan University, Shanghai, 200032, China.
Xiaoyu TongDepartment of Integrative Medicine and Neurobiology, School of Basic Medical Sciences, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Fudan University, Shanghai, 200032, China.
Yi TianDepartment of Ophthalmology & Visual Science, Eye & ENT Hospital, Shanghai Medical College, Fudan University, Shanghai, 200031, China.
Yuning ChenReproductive Medicine Center, Zhongshan Hospital, Shanghai Medical College, Fudan University, Shanghai, 200040, China.
Yicong WangDepartment of Integrative Medicine and Neurobiology, School of Basic Medical Sciences, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Fudan University, Shanghai, 200032, China.
Yan XiaoDepartment of Integrative Medicine and Neurobiology, School of Basic Medical Sciences, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Fudan University, Shanghai, 200032, China.
Hongfang YangDepartment of Ophthalmology & Visual Science, Eye & ENT Hospital, Shanghai Medical College, Fudan University, Shanghai, 200031, China. hongfang_yang@126.com.
Yi FengDepartment of Integrative Medicine and Neurobiology, School of Basic Medical Sciences, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Fudan University, Shanghai, 200032, China. fengyi17@fudan.edu.cn.
Xinghuai SunDepartment of Ophthalmology & Visual Science, Eye & ENT Hospital, Shanghai Medical College, Fudan University, Shanghai, 200031, China. xhsun@shmu.edu.cn.

Funding

Clinical Research Plan of SHDC SHDC2020CR6029Development Project of Shanghai Peak Disciplines-Integrated Chinese and Western Medicine 20180101Fuqing Scholar student scientific research program FQXZ202210ANational Key Research and Development Program of China 2020YFA0112700Shanghai Municipal Health Commission 20214Y0073State Key Program of National Natural Science Foundation of China 82030027
6 · The paper itself

Abstract

Acute ocular hypertension (AOH), a major cause of progressive irreversible vision loss, showed significant retinal ganglion cell (RGC) degeneration as well as selective RGC vulnerability upon functional tests, yet the underlyding mechanisms remain incompletely understood. Here, we report the activation of transient receptor potential ankyrin 1 (TRPA1), a mechanosensitive ion channel on RGCs under AOH by RT-qPCR, Western blot, immunofluorescent, flow cytometry and calcium imaging tests. Downstream CaMKII/CREB pathways were evaluated, showing significantly elevated phospho-CaMKII and down-regulated phospho-CREB1 under AOH. Further, by applying a modified whole-brain clearing method, the region-specific RGC axonal damage among lateral geniculate nuclei (LGN) subregions were adopted to detect the involvement of TRPA1 on selective RGC vulnerability. Together with tissue-specific knock-out or channel inhibition test, the exacerbation of TRPA1 on RGC degeneration as well as selective injury tendency under AOH was confirmed. In virtue of our modified whole-brain clearing method, our data confirmed the innovational method to study the mechanisms behind selective vulnerability of neuronal cells, and in the meantime revealed the potential therapeutic opportunity of targeting TRPA1 for patients suffering from AOH attack.

Indexed as

Ocular HypertensionRetinal Ganglion CellsTRPA1 Cation ChannelAnimalsCalcium-Calmodulin-Dependent Protein Kinase Type 2MaleMiceMice, Inbred C57BLMice, KnockoutCalcium-Calmodulin-Dependent Protein Kinase Type 2TRPA1 Cation ChannelTrpa1 protein, mouseAcute ocular hypertensionNeuronal selective vulnerabilityRGC central projectionTissue optical clearingTRPA1

Identifiers

PMID40186313
PMCPMC11971892

What OpenQuestion 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 OpenQuestion graph.