ArticleCardiovascular diabetology2026
Divergent mitochondrial and fibrotic signatures in atrial fibrillation: insights from organoids and GEO data.
Article in Cardiovascular diabetology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundAtrial fibrillation (AF) remains a major clinical burden because structural and metabolic remodeling, particularly mitochondrial dysfunction and fibrosis, often persists beyond rhythm control. Human-relevant models that disentangle these axes and connect them to patient data are limited.
methodsHuman atrial organoids were exposed to two AF-relevant stressors: rapid pacing (FP) and angiotensin II (AngII). We assessed mitochondrial and fibrotic remodeling by transcript/protein analyses, imaging, and contractility readouts, and benchmarked organoid responses against four public AF transcriptomic datasets (GEO: GSE128188, GSE138252, GSE222793, GSE239321). Statistical analyses used predefined contrasts versus matched controls with multiple-testing correction.
resultsFP predominantly suppressed mitochondrial biogenesis/oxidative programs and increased stress-response features, resembling signatures observed in AF with heart failure (e.g., downregulation of mitochondrial regulators and altered cytochrome c patterns). AngII elicited stronger profibrotic signaling with a mixed mitochondrial response, mirroring profiles more typical of AF without heart failure. Both stressors impaired organoid contractility. Protein and immunostaining corroborated mitochondria-fibrosis crosstalk, with changes in PGC1α and cytochrome c alongside increased extracellular matrix deposition and myofibroblast markers (COL1A1, αSMA), consistent with stimulus-specific but partially overlapping remodeling trajectories.
conclusionDistinct AF-relevant stressors drive divergent mitochondrial and fibrotic remodeling in human atrial organoids that recapitulate key features of patient datasets. These organoid models provide a translational platform to prioritize mitochondria-targeted and antifibrotic interventions and to inform biomarker development for residual dysfunction in AF.
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