Evidence map›Paper›PMID 41577749›Full record

ArticleCommunications biology2026

40 Hz flicker preconditioning protects nonarteritic anterior ischemic optic neuropathy via adenosine signaling.

Lingya Su, Ruojun Lu, Lijuan Huang, Manli Jia, Jing Liao, Libin Huang, Youru Wu, Tao Shi, Xianghang He, Yan He and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Communications biology, 2026. 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
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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

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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

13 authors.

Lingya SuThe Molecular Neuropharmacology Laboratory and the Eye-Brain Research Center, State Key Laboratory of Eye Health, Eye Hospital, Wenzhou Medical University, Wenzhou, China.
Ruojun LuThe Molecular Neuropharmacology Laboratory and the Eye-Brain Research Center, State Key Laboratory of Eye Health, Eye Hospital, Wenzhou Medical University, Wenzhou, China.
Lijuan HuangThe Molecular Neuropharmacology Laboratory and the Eye-Brain Research Center, State Key Laboratory of Eye Health, Eye Hospital, Wenzhou Medical University, Wenzhou, China.
Manli JiaThe Molecular Neuropharmacology Laboratory and the Eye-Brain Research Center, State Key Laboratory of Eye Health, Eye Hospital, Wenzhou Medical University, Wenzhou, China.
Jing LiaoThe Molecular Neuropharmacology Laboratory and the Eye-Brain Research Center, State Key Laboratory of Eye Health, Eye Hospital, Wenzhou Medical University, Wenzhou, China.
Libin HuangThe Molecular Neuropharmacology Laboratory and the Eye-Brain Research Center, State Key Laboratory of Eye Health, Eye Hospital, Wenzhou Medical University, Wenzhou, China.
Youru WuThe Molecular Neuropharmacology Laboratory and the Eye-Brain Research Center, State Key Laboratory of Eye Health, Eye Hospital, Wenzhou Medical University, Wenzhou, China.
Tao ShiThe Molecular Neuropharmacology Laboratory and the Eye-Brain Research Center, State Key Laboratory of Eye Health, Eye Hospital, Wenzhou Medical University, Wenzhou, China.
Xianghang HeThe Molecular Neuropharmacology Laboratory and the Eye-Brain Research Center, State Key Laboratory of Eye Health, Eye Hospital, Wenzhou Medical University, Wenzhou, China.
Yan HeThe Molecular Neuropharmacology Laboratory and the Eye-Brain Research Center, State Key Laboratory of Eye Health, Eye Hospital, Wenzhou Medical University, Wenzhou, China.
Zuhua SunSchool of Ophthalmology & Optometry and Eye Hospital, Wenzhou Medical University, Wenzhou, China.
Jiang-Fan ChenThe Molecular Neuropharmacology Laboratory and the Eye-Brain Research Center, State Key Laboratory of Eye Health, Eye Hospital, Wenzhou Medical University, Wenzhou, China. chenjf555@gmail.com.ORCID http://orcid.org/0000-0002-0446-3956
Ying GaoThe Molecular Neuropharmacology Laboratory and the Eye-Brain Research Center, State Key Laboratory of Eye Health, Eye Hospital, Wenzhou Medical University, Wenzhou, China. gaoying@wmu.edu.cn.ORCID http://orcid.org/0000-0002-7014-2392

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nonarteritic anterior ischemic optic neuropathy (NAION) is a leading cause of sudden, painless vision loss in the elderly, yet no proven intervention exists. Ischemic preconditioning (IPC) is a promising neuroprotective strategy, but defining an effective clinical protocol remains a major challenge in fulfilling its translational potential. We recently discovered that 40 Hz flicker induces extracellular adenosine, a key neurochemical underpinning of IPC, in the visual pathway, suggesting a previously unexplored non-invasive IPC approach. Here, we demonstrated that 3-day 40 Hz flicker preconditioning significantly protected against NAION by reducing retinal ganglion cell loss, preserving ganglion cell layer structure, improving visual function, and attenuating microglial activation. Protection was strongest when ischemia occurred 12 hours after preconditioning, remained moderate at 24 hours, and persisted for at least 4 weeks. This effect was specific to preconditioning and flicker frequency-dependent (effective at 40 Hz, but not at 20 Hz or 80 Hz). Furthermore, neuroprotection by 40 Hz flicker was abolished by treatment with the equilibrative nucleoside transporter inhibitor dipyridamole and the A

Indexed as

AdenosineIschemic PreconditioningOptic Neuropathy, IschemicSignal TransductionAnimalsMaleMiceRetinal Ganglion CellsAdenosine

Identifiers

PMID41577749
PMCPMC12932722

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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.