https://transhumanist.ru/index.php?action=history&feed=atom&title=ASIC2ASIC2 - История изменений2026-10-21T14:25:55ZИстория изменений этой страницы в викиMediaWiki 1.43.6https://transhumanist.ru/index.php?title=ASIC2&diff=4459&oldid=prevOdysseusBot: Новая страница: «Acid-sensing ion channel 2 (ASIC2) (Amiloride-sensitive brain sodium channel) (Amiloride-sensitive cation channel 1, neuronal) (Amiloride-sensitive cation channel...»2021-04-29T19:19:14Z<p>Новая страница: «Acid-sensing ion channel 2 (ASIC2) (Amiloride-sensitive brain sodium channel) (Amiloride-sensitive cation channel 1, neuronal) (Amiloride-sensitive cation channel...»</p>
<p><b>Новая страница</b></p><div>Acid-sensing ion channel 2 (ASIC2) (Amiloride-sensitive brain sodium channel) (Amiloride-sensitive cation channel 1, neuronal) (Amiloride-sensitive cation channel neuronal 1) (Brain sodium channel 1) (BNC1) (BNaC1) (Mammalian degenerin homolog) (MDEG) [ACCN] [ACCN1] [BNAC1] [MDEG]<br />
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==Publications==<br />
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{{medline-entry<br />
|title=Acidotoxicity and acid-sensing ion channels contribute to motoneuron degeneration.<br />
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/23306556<br />
|abstract=Amyotrophic lateral sclerosis (ALS) is a fatal neurological condition with no cure. Mitochondrial dysfunction, Ca(2 ) overloading and local hypoxic/ischemic environments have been implicated in the pathophysiology of ALS and are conditions that may initiate metabolic acidosis in the affected tissue. We tested the hypothesis that acidotoxicity and acid-sensing ion channels (ASICs) are involved in the pathophysiology of ALS. We found that motoneurons were selectively vulnerable to acidotoxicity in vitro, and that acidotoxicity was partially reduced in asic1a-deficient motoneuron cultures. Cross-breeding of [[SOD1]](G93A) ALS mice with asic1a-deficient mice delayed the onset and progression of motor dysfunction in [[SOD1]] mice. Interestingly, we also noted a strong increase in [[ASIC2]] expression in motoneurons of [[SOD1]] mice and sporadic ALS patients during disease progression. Pharmacological pan-inhibition of ASIC channels with the lipophilic amiloride derivative, 5-(N,N-dimethyl)-amiloride hydrochloride, potently protected cultured motoneurons against acidotoxicity, and, given post-symptom onset, significantly improved lifespan, motor performance and motoneuron survival in [[SOD1]] mice. Together, our data provide strong evidence for the involvement of acidotoxicity and ASIC channels in motoneuron degeneration, and highlight the potential of ASIC inhibitors as a new treatment approach for ALS.<br />
|mesh-terms=* Acid Sensing Ion Channels<br />
* Acids<br />
* Amiloride<br />
* Amyotrophic Lateral Sclerosis<br />
* Animals<br />
* Apoptosis<br />
* Cells, Cultured<br />
* Disease Models, Animal<br />
* Humans<br />
* Longevity<br />
* Male<br />
* Mice<br />
* Mice, Inbred C57BL<br />
* Mice, Knockout<br />
* Mice, Transgenic<br />
* Motor Neurons<br />
* Mutation<br />
* Superoxide Dismutase<br />
* Superoxide Dismutase-1<br />
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|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3595486<br />
}}</div>OdysseusBot