ArticleCell death and differentiation2013
Intracellular ASIC1a regulates mitochondrial permeability transition-dependent neuronal death.
Article in Cell death and differentiation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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.
The trial behind it
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Who cites it
29 citing papers in PubMed, 49 citations in OpenAlex.
- Acid-sensing ion channels in ischemic stroke: amplifying and constraining neuronal injury in a phase-specific framework.Pflugers Archiv : European journal of physiology · 2026Review
- Acid-sensing ion channels in the vasculature: emerging roles in systemic and pulmonary circulations.Pflugers Archiv : European journal of physiology · 2026Review
- The multifaceted role of ASICs channels into the nervous system and their potential use as a therapeutic target for neuro-disorders.Journal of neural transmission (Vienna, Austria : 1996) · 2026Review
- Mitochondrial acid-sensing ion channel 1a deficiency induces mitochondrial dysfunction in pulmonary arterial smooth muscle cells.American journal of physiology. Lung cellular and molecular physiology · 2026Article
- The relationship between acid-sensing ion channel, ASIC2, and oncogenic β-catenin signaling in ovarian cancer.Scientific reports · 2025Article
- Selective blockade of acid-sensing ion channel 1a can provide substantial hippocampal neuroprotection.Frontiers in cell and developmental biology · 2025Article
- Review
- Acid-sensing ion channel 1a modulation of apoptosis in acidosis-related diseases: implications for therapeutic intervention.Cell death discovery · 2023Review
- Acid-sensing ion channel 1a: a novel target in Alzheimer's disease?Neural regeneration research · 2023Article
- Ketogenic Diet Alleviates Hippocampal Neurodegeneration Possibly via ASIC1a and the Mitochondria-Mediated Apoptotic Pathway in a Rat Model of Temporal Lobe Epilepsy.Neuropsychiatric disease and treatment · 2022Article
- Acid-Sensing Ion Channels and Mechanosensation.International journal of molecular sciences · 2021Review
- Dual-process brain mitochondria isolation preserves function and clarifies protein composition.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- The Role of ASIC1a in Epilepsy: A Potential Therapeutic Target.Current neuropharmacology · 2021Review
- DEG/ENaC Ion Channels in the Function of the Nervous System: From Worm to Man.Advances in experimental medicine and biology · 2021Article
- Complementary Oligonucleotide Conjugated Multicolor Carbon Dots for Intracellular Recognition of Biological Events.ACS applied materials & interfaces · 2020Article
- ASIC1a channels regulate mitochondrial ion signaling and energy homeostasis in neurons.Journal of neurochemistry · 2020Article
- The acid-sensing ion channel ASIC1a mediates striatal synapse remodeling and procedural motor learning.Science signaling · 2018Article
- Acid-sensing ion channel 1a mediates acid-induced inhibition of matrix metabolism of rat articular chondrocytes via the MAPK signaling pathway.Molecular and cellular biochemistry · 2018Article
- Hi1a as a Novel Neuroprotective Agent for Ischemic Stroke by Inhibition of Acid-Sensing Ion Channel 1a.Translational stroke research · 2018Article
- Targeted Acid-Sensing Ion Channel Therapies for Migraine.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2018Review
Corrections and comments
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Authors and funding
10 authors at 6 institutions in 4 countries.
Funding
Abstract
Acid-sensing ion channel 1a (ASIC1a) is the key proton receptor in nervous systems, mediating acidosis-induced neuronal injury in many neurological disorders, such as ischemic stroke. Up to now, functional ASIC1a has been found exclusively on the plasma membrane. Here, we show that ASIC1a proteins are also present in mitochondria of mouse cortical neurons where they are physically associated with adenine nucleotide translocase. Moreover, purified mitochondria from ASIC1a(-/-) mice exhibit significantly enhanced Ca(2+) retention capacity and accelerated Ca(2+) uptake rate. When challenged with hydrogen peroxide (H2O2), ASIC1a(-/-) neurons are resistant to cytochrome c release and inner mitochondrial membrane depolarization, suggesting an impairment of mitochondrial permeability transition (MPT) due to ASIC1a deletion. Consistently, H2O2-induced neuronal death, which is MPT dependent, is reduced in ASIC1a(-/-) neurons. Additionally, significant increases in mitochondrial size and oxidative stress levels are detected in ASIC1a(-/-) mouse brain, which also displays marked changes (>2-fold) in the expression of mitochondrial proteins closely related to reactive oxygen species signal pathways, as revealed by two-dimensional difference gel electrophoresis followed by mass spectrometry analysis. Our data suggest that mitochondrial ASIC1a may serve as an important regulator of MPT pores, which contributes to oxidative neuronal cell death.
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Registered trials
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.