English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

The dysregulation of K +  channels is a hallmark of pulmonary arterial hypertension (PAH). Herein, the channelome was analyzed in lungs of patients with PAH in a public transcriptomic database. Sixty six (46%) mRNA encoding cationic channels were dysregulated in PAH with most of them downregulated (83%). The principal component analysis indicated that dysregulated cationic channel expression is a signature of the disease. Changes were very similar in idiopathic, connective tissue disease and congenital heart disease associated PAH. This analysis 1) is in agreement with the widely recognized pathophysiological role of TASK1 and K V 1.5, 2) supports previous preliminary reports pointing to the dysregulation of several K +  channels including the downregulation of K V 1.1, K V 1.4, K V 1.6, K V 7.1, K V 7.4, K V 9.3 and TWIK2 and the upregulation of K Ca 1.1 and 3) points to other cationic channels dysregulated such as Kv7.3, TALK2, Ca V 1 and TRPV4 which might play a pathophysiological role in PAH. The significance of other changes found in Na +  and TRP channels remains to be investigated.

Transcriptomic profile of cationic channels in human pulmonary arterial hypertension