ArticleJournal of inflammation research2026
Identification of PANoptosis-Related Biomarkers in Hypertrophic Cardiomyopathy: Insights from Multi-Omics Analysis.
Article in Journal of inflammation research, 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
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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.
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Who cites it
1 citing paper in PubMed.
- Evidence for a role of adverse sarcomere signaling in atrial fibrillation induction.Journal of molecular and cellular cardiology plus · 2026Review
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Authors and funding
8 authors.
Funding
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Abstract
Background: Hypertrophic cardiomyopathy (HCM) is a common inherited cardiomyopathy characterized by ventricular hypertrophy, fibrosis, and increased risk of sudden cardiac death. However, the underlying molecular pathways contributing to its progression remain incompletely defined. PANoptosis, a newly defined inflammatory form of programmed cell death integrating pyroptosis, apoptosis, and necroptosis, has been implicated in cardiac injury and may represent a convergent mechanism linking inflammation and myocardial remodeling, but remains uninvestigated in HCM. Methods: Transcriptomic profiles from HCM and control hearts were analyzed to identify differentially expressed PANoptosis-related genes. A nine-gene diagnostic panel was constructed using a comprehensive multi-algorithm machine learning framework integrating ensemble, kernel-based, and regularized regression models, and validated in external cohorts. Molecular subtypes were identified through consensus clustering. Immune infiltration, functional enrichment, and ceRNA regulatory networks were evaluated. Single-nucleus RNA sequencing localized gene expression to specific cardiac cell types. Cell-cell communication analysis explored intercellular signaling. Experimental validation was performed in a murine HCM model using echocardiography, histology, and RT-qPCR. Molecular docking assessed therapeutic potential of candidate compounds. Finally, molecular docking and target prediction were applied to explore potential therapeutic compounds acting on the PANoptosis axis. Results: Nine PANoptosis-related genes (S100A9, GADD45A, IER3, STAT3, SFRP1, PHLDA1, JAK2, MYC, S100A8) showed high diagnostic performance (AUC > 0.95). Two molecular subtypes displayed distinct immune and metabolic signatures. PANoptosis genes correlated with T cells, macrophages, and dendritic cells. CellChat analysis revealed PDGF-mediated signaling between cardiomyocytes and fibroblasts. Key genes exhibited cell-type-specific expression. In vivo validation confirmed gene expression trends. Moreover, folic acid and tretinoin exhibited favorable docking affinity with core targets, suggesting potential therapeutic relevance. Conclusion: This study provides the first systematic evidence linking PANoptosis to the molecular pathogenesis of HCM. PANoptosis contributes to HCM pathogenesis and immune remodeling, and the identified biomarkers demonstrate translational potential as diagnostic indicators and therapeutic targets. The integrated analysis highlights novel PANoptotic signaling axes that may guide future precision diagnosis and intervention strategies for HCM.
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