Atrial fibrillation in goats was associated with enrichment of oxidative phosphorylation subunits and implicated HSPA9 as a central regulatory hub coordinating dysregulation of Complex I and III.
Bioinformatic analysis of goat left atrial tissue reveals a coordinated mitochondrial adaptation in atrial fibrillation, highlighting HSPA9 as a key regulatory hub for oxidative phosphorylation.
Abstract Atrial fibrillation (AF) increases energy demand in atrial myocytes, yet the mitochondrial mechanisms underlying this stress remain poorly defined. Using previously published proteomic data from left atrial tissue of AF and sham-operated goats, we performed organelle-specific bioinformatic analyses of the mitochondrial fraction. Over-representation and consensus pathway analyses consistently highlighted enrichment of oxidative phosphorylation (OXPHOS) subunits. Gene set enrichment and network analyses implicated Heat Shock Protein Family A Member 9 (HSPA9) as a potentially central regulatory hub coordinating the dysregulation of Complex I and III subunits, with 69% of regulatory relationships showing pathway concordance. These results indicate a coordinated, system-wide mitochondrial adaptation in AF, integrating energy production, proteostasis, and respiratory chain regulation.
Ayagama et al. (Thu,) conducted a other in Atrial fibrillation. Atrial fibrillation vs. Sham-operated was evaluated on Mitochondrial fraction proteomic signatures. Atrial fibrillation in goats was associated with enrichment of oxidative phosphorylation subunits and implicated HSPA9 as a central regulatory hub coordinating dysregulation of Complex I and III.