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Peer-reviewedCC BY-NC-NDPflugers Archiv : European journal of physiology

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

  • Ke Lai1
  • Lu-Yang Wang2,3
  1. 1Department of Otorhinolaryngology, Shanghai Sixth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200032, China. [email protected].
  2. 2Program in Neuroscience and Mental Health, SickKids Research Institute, Toronto, M5G 1X8, Canada. [email protected].
  3. 3Department of Physiology, University of Toronto, Toronto, M5S 1A1, Canada. [email protected].
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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.

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Cite

BibTeXRIS
BibTeX
@article{lai2026asic1a,
  title = {{ASIC1a as an integrating node in ischemic neurotoxicity: crosstalk with NMDAR and TRPM signaling.}},
  author = {Ke Lai and Lu-Yang Wang},
  journal = {Pflugers Archiv : European journal of physiology},
  year = {2026},
  month = oct,
  doi = {10.1007/s00424-026-03225-5},
  url = {https://europepmc.org/article/MED/42897310},
  note = {CC BY-NC-ND},
}
RIS
TY  - JOUR
TI  - ASIC1a as an integrating node in ischemic neurotoxicity: crosstalk with NMDAR and TRPM signaling.
AU  - Ke Lai
AU  - Lu-Yang Wang
PY  - 2026
DA  - 2026/10/20
JO  - Pflugers Archiv : European journal of physiology
DO  - 10.1007/s00424-026-03225-5
UR  - https://europepmc.org/article/MED/42897310
AB  - 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.
SN  - 0031-6768
SN  - 1432-2013
ER  -