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Interleukin-1β Drives Disease Progression in Arrhythmogenic Cardiomyopathy
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DOI：10.1016/j.jacbts.2026.101542.png)
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Abstract
En 中文
• snRNAseq of human ACM hearts reveals increased proportions of distinct inflammatory myeloid cells and activated fibroblasts. • Spatial transcriptomics analysis of human ACM reveals distinct spatial niches made up of inflammatory myeloid cells and activated fibroblasts in areas of tissue damage and fibrosis referred to as lesions. • Inhibition of IL1B signaling using a neutralizing antibody leads to significant attenuation of ACM pathogenesis in the Dsg2mut/mut mouse model of ACM.
Keywords:
arrhythmogenic cardiomyopathy
cardioimmunology
CCR2+ macrophages
myocardial inflammation
ACM
arrhythmogenic cardiomyopathy
Cx43
connexin-43
Fib1
fibroblast cell state 1
H&E
hematoxylin and eosin
IgG
immunoglobulin G
Mac1
macrophage state 1
mFib1
murine fibroblast cluster 1
MI
myocardial infarct
mMac1
murine macrophage state 1
mMono1
murine monocyte state 1
NFκB
nuclear factor κB
snRNAseq
single nucleus RNA sequencing
UMAP
uniform manifold approximation and projection
WT
wild type
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