ArticleRedox biology2026
Resistance to atrial fibrillation domestication and mitochondrial dysfunction in sheep: a potential key role of the TCA cycle and mitochondrial redox state.
Article in Redox biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- The clinical pathophysiology of atrial fibrillation: outstanding questions from bedside to bench and back.Physiological reviews · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
25 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAtrial fibrillation (AF) often progresses from paroxysmal to more stable forms. It is well-recognized that patients vary in their AF progression, but the underlying mechanisms remain unclear. This work, performed in a sheep AF-model, aimed to identify atrial redox and energetic status differences between animals developing stable AF (AF-S) versus those resistant to AF-stabilization (AF-R).
methodsAF was induced with bursts of atrial tachystimulation, maintained whenever sinus rhythm resumed, and monitored with telemetry. Electrophysiological and structural remodeling were assessed via contact mapping, and histology, respectively. Proteomic, metabolomic, enzymatic, and bioenergetic remodeling were evaluated using left atrial appendage (LAA) tissues and isolated LAA mitochondria. Healthy rats were used to investigate whether a metabolic challenge stabilizes electrically induced AF episodes.
resultsAF-S (N = 12) sheep developed stable AF after 13 days on average, whereas AF-R (N = 8) sheep failed to develop self-sustained AF despite 120 days of tachypacing. Contact mapping and histological analysis revealed that AF-S animals presented reduced atrial conduction velocity, and increased endomysial fibrosis. Metabolic analysis showed significant differences in tricarboxylic acid cycle (TCA) enzymes activities and a 45% succinate content increase in AF-S LAA versus AF-R. AF-S mitochondria showed abnormal succinate oxidation, decreased ATP synthesis rate, and increased ROS emission. The ratios of ATP/ADP, NAD
conclusionsAF-S sheep showed TCA cycle, energetic and redox adaptations compared to AF-R. In this animal model, TCA cycle remodeling and associated redox and energetic responses determined the resistance to AF domestication, with potential relevance to identify new mechanistic determinants of AF progression in humans.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.