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Life sciences · Journal article
Biology Direct · August 11, 2026
Early or partial results. Treat as a signal, not a conclusion.
This study identifies an ICAM1-expressing inflammatory fibroblast state enriched in atrial fibrillation samples (17.3% of AF fibroblasts) and associates it with inflammatory and matrix-remodeling gene programs. Using mouse diet-induced obesity, human tissue RNA fluorescence, protein quantification, and in vitro fibroblast knockdown and overexpression experiments, the authors establish that ICAM1 perturbation alters fibroblast migration and matrix protein expression and link this to TNXB-dependent pathways. However, the work remains mechanistic; the authors themselves acknowledge that further fibroblast-specific and clinically annotated studies are needed to define causality and translational relevance.
Mechanistic study combining human transcriptomics reanalysis, mouse disease model, tissue analysis, and in vitro fibroblast experiments. Human left atrial samples from AF and sinus rhythm patients (dataset characteristics not stated); C57BL/6J mice with diet-induced obesity or normal diet; primary human cardiac fibroblasts (cell line source not specified).. Intervention: Diet-induced obesity in mice; ICAM1 knockdown and TNXB lentiviral overexpression in primary human cardiac fibroblasts; burst pacing in isolated mouse hearts.. Compared with: Normal-diet control mice; non-transfected or scrambled-control fibroblasts; TGF-β1 stimulation without overexpression..
ICAM1⁺ inflammatory fibroblast state identified in reanalysis of human left atrial scRNA-seq; represented 17.3% of fibroblasts in AF samples but not detected in sinus rhythm samples Diet-induced obesity mice showed higher susceptibility to burst pacing–induced AF-like atrial tachyarrhythmia (5/8 vs. 0/8 normal diet controls; Fisher's exact P = 0.0256) ICAM1 protein increased in CD140a-enriched atrial fibroblast fractions from DIO mice (relative ICAM1/β-actin: 2.70 ± 0.46 vs. 1.00 ± 0.15; P = 0.0001)
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This work provides mechanistic insight into a potential fibroblast subtype in atrial fibrillation and identifies ICAM1 as a node in inflammatory-fibrotic remodeling. However, no clinical endpoints, patient outcomes, or therapeutic interventions are tested; the findings remain preclinical and require validation in larger clinical cohorts and functional studies to establish whether targeting ICAM1 would benefit AF patients.
Single-centre mechanistic study combining human transcriptomics reanalysis with mouse disease modelling and in vitro fibroblast manipulation; identifies a putative fibroblast state and pathway associations but lacks clinical endpoints and acknowledges need for further work to establish causality and clinical relevance.
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Quoted from the source exactly as published.
This work provides mechanistic insight into a potential fibroblast subtype in atrial fibrillation and identifies ICAM1 as a node in inflammatory-fibrotic remodeling. However, no clinical endpoints, patient outcomes, or therapeutic interventions are tested; the findings remain preclinical and require validation in larger clinical cohorts and functional studies to establish whether targeting ICAM1 would benefit AF patients.
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Atrial fibrillation (AF) is associated with inflammatory and fibrotic atrial remodeling, but the fibroblast states connecting these processes remain incompletely defined. ICAM1 is a key inflammatory adhesion molecule, yet its cell-state context within atrial fibroblast heterogeneity remains unclear. Reanalysis of human left atrial single-cell RNA sequencing data identified an ICAM1⁺ inflammatory fibroblast state that was not detected among fibroblasts from sinus rhythm samples in this dataset and represented 17.3% of fibroblasts in AF samples. Trajectory inference, pathway enrichment, and co-expression network analysis associated this state with inflammatory and matrix-remodeling programs. In diet-induced obesity (DIO) mice, susceptibility to burst pacing–induced AF-like atrial tachyarrhythmia episodes was higher than in normal-diet controls (5/8 vs. 0/8 mice; Fisher’s exact P = 0.0256), accompanied by left atrial remodeling. RNA fluorescence in situ hybridization supported increased Icam1 expression in Tcf21 ⁺ fibroblast-associated stromal cells. ICAM1 protein was increased in CD140a-enriched atrial fibroblast fractions from DIO mice (relative ICAM1/β-actin: 2.70 ± 0.46 vs. 1.00 ± 0.15; P = 0.0001). In primary human cardiac fibroblasts, ICAM1 knockdown reduced migration under TGF-β1-stimulated conditions (49.90 ± 1.63% vs. 20.44 ± 1.51% wound closure; P < 0.0001), and reduced α-SMA and Collagen I fluorescence signals. Lentiviral TNXB overexpression partially restored Fibronectin and Collagen I expression under ICAM1-knockdown conditions (Fibronectin: 2.26 ± 0.21-fold vs. 4.11 ± 0.28-fold, P < 0.0001; Collagen I: 1.09 ± 0.06-fold vs. 1.54 ± 0.09-fold, P = 0.0004). This study identifies an AF-enriched ICAM1⁺ inflammatory fibroblast state associated with inflammatory–matrix remodeling programs. The findings support Icam1 upregulation in fibroblast-associated atrial stromal cells during DIO-associated remodeling and link ICAM1 perturbation to altered fibroblast migration and selected TNXB-associated matrix-protein readouts. Further fibroblast-specific and clinically annotated studies are needed to define causality and translational relevance.
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