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	<title>ADORA2B - История изменений</title>
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		<title>OdysseusBot: Новая страница: «Adenosine receptor A2b  ==Publications==  {{medline-entry |title=Adenosine A2B receptor: A pathogenic factor and a therapeutic target for sensorineural hearing lo...»</title>
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		<summary type="html">&lt;p&gt;Новая страница: «Adenosine receptor A2b  ==Publications==  {{medline-entry |title=Adenosine A2B receptor: A pathogenic factor and a therapeutic target for sensorineural hearing lo...»&lt;/p&gt;
&lt;p&gt;&lt;b&gt;Новая страница&lt;/b&gt;&lt;/p&gt;&lt;div&gt;Adenosine receptor A2b&lt;br /&gt;
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==Publications==&lt;br /&gt;
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{{medline-entry&lt;br /&gt;
|title=Adenosine A2B receptor: A pathogenic factor and a therapeutic target for sensorineural hearing loss.&lt;br /&gt;
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33131093&lt;br /&gt;
|abstract=Over 466 million people worldwide are diagnosed with hearing loss (HL). About 90% of HL cases are sensorineural HL (SNHL) with treatments limited to hearing aids and cochlear implants with no FDA-approved drugs. Intriguingly, [[ADA]]-deficient patients have been reported to have bilateral SNHL, however, its underlying cellular and molecular basis remain unknown. We report that Ada  mice, phenocopying [[ADA]]-deficient humans, displayed SNHL. Ada  mice cochlea with elevated adenosine caused substantial nerve fiber demyelination and mild hair cell loss. [[ADA]] enzyme therapy in these mice normalized cochlear adenosine levels, attenuated SNHL, and prevented demyelination. Additionally, [[ADA]] enzyme therapy rescued SNHL by restoring nerve fiber structure in Ada  mice post two-week drug withdrawal. Moreover, elevated cochlear adenosine in untreated mice was associated with enhanced Adora2b gene expression. Preclinically, [[ADORA2B]]-specific antagonist treatment in Ada  mice significantly improved HL, nerve fiber density, and myelin compaction. We also provided genetic evidence that [[ADORA2B]] is detrimental for age-related SNHL by impairing cochlear myelination in WT aged mice. Overall, understanding purinergic molecular signaling in SNHL in Ada  mice allows us to further discover that [[ADORA2B]] is also a pathogenic factor underlying aged-related SNHL by impairing cochlear myelination and lowering cochlear adenosine levels or blocking [[ADORA2B]] signaling are effective therapies for SNHL.&lt;br /&gt;
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|keywords=* ADA-deficiency&lt;br /&gt;
* adenosine deaminase deficiency&lt;br /&gt;
* aging&lt;br /&gt;
* myelin protein zero&lt;br /&gt;
* myelination&lt;br /&gt;
|full-text-url=https://sci-hub.do/10.1096/fj.202000939R&lt;br /&gt;
}}&lt;/div&gt;</summary>
		<author><name>OdysseusBot</name></author>
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