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

Myoblast fusion depends on mitochondrial integrity and intracellular Ca 2+ signaling regulated by various ion channels. In this study, we investigated the ionic currents associated with [Ca 2+ ] i regulation in normal and mitochondrial DNA-depleted (ρ0) L6 myoblasts. The ρ0 myoblasts showed impaired myotube formation. The inwardly rectifying K + current (I Kir ) was largely decreased with reduced expression of KIR2.1, whereas the voltage-operated Ca 2+ channel and Ca 2+ -activated K + channel currents were intact. Sustained inhibition of mitochondrial electron transport by antimycin A treatment (24 h) also decreased the I Kir . The ρ0 myoblasts showed depolarized resting membrane potential and higher basal [Ca 2+ ] i . Our results demonstrated the specific downregulation of I Kir by dysfunctional mitochondria. The resultant depolarization and altered Ca 2+ signaling might be associated with impaired myoblast fusion in ρ0 myoblasts.

Mitochondrial dysfunction reduces the activity of KIR2.1 K+ channel in myoblasts via impaired oxidative phosphorylation