ASIC1a as an integrating node in ischemic neurotoxicity: crosstalk with NMDAR and TRPM signaling.

Ke Lai, Lu-Yang Wang

Abstract readReview

In one paragraph

Review in Pflugers Archiv : European journal of physiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed

–field-weighted citation impact

1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

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0 citing papers in PubMed.

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4 · The record

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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

2 authors.

Ke LaiDepartment of Otorhinolaryngology, Shanghai Sixth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200032, China. ilaike@sjtu.edu.cn.

Lu-Yang WangProgram in Neuroscience and Mental Health, SickKids Research Institute, Toronto, M5G 1X8, Canada. luyang.wang@utoronto.ca.

Funding

Canada Research Chairs CRC-95-232466CIHR 202309PJT-505732; 202403PJT-518084National Natural Science Foundation of China 82522024Natural Sciences and Engineering Research Council of Canada RGPIN-2022-05425

6 · The paper itself

Abstract

Ischemic stroke triggers acidosis, glutamate excitotoxicity and oxidative stress, which converge to disturb ionic homeostasis through several cation channels, including acid-sensing ion channel 1a (ASIC1a), N-methyl-D-aspartate receptors (NMDARs) and transient receptor potential melastatin (TRPM) channels. Emerging evidence suggests that ASIC1a functions as a context-dependent integrating node: protons directly gate ASIC1a, glutamate and bilirubin-associated signaling can modulate ASIC1a-dependent injury pathways. ASIC1a directly couples with NMDAR-dependent signaling and indirectly engages TRPM-associated pathways. Here, we discuss the mechanistic basis, therapeutic potential and unresolved questions regarding ASIC1a-associated signaling in ischemic brain injury.

Indexed as

Acid Sensing Ion ChannelsBrain IschemiaReceptors, N-Methyl-D-AspartateTRPM Cation ChannelsAnimalsHumansSignal TransductionAcid Sensing Ion ChannelsASIC1 protein, humanReceptors, N-Methyl-D-AspartateTRPM Cation ChannelsAcid-sensing ion channelsIschemic strokeNeurotoxicityN-methyl-D-aspartate receptorsTRPM channels

Identifiers

PMID42897310

DOI10.1007/s00424-026-03225-5

PMCPMC13680530

What OpenQuestion holds

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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.