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LDLR-OPN Interaction Drives COVID-19 Myocarditis Through Monocyte Recruitment
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DOI：10.1016/j.jacbts.2026.101553.png)
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Abstract
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• Cardiac-specific LDLR overexpression combined with chimeric SARS-CoV-2 infection in K18-hACE2 mice establishes a BSL-2–compatible model achieving 100% penetrance with macrophage-predominant infiltration and cardiomyocyte necrosis that recapitulates human COVID-19 myocarditis; IDOL-mediated LDLR degradation completely abrogates the phenotype. • A novel high-affinity LDLR-OPN interaction (mapped to CR2-CR5 domains) drives monocyte recruitment. OPN-knockout macrophages fail to migrate toward LDLR-overexpressing cardiomyocytes, confirming the functional indispensability of this axis. • Among inflammatory cell death pathways, only GSDMD-mediated pyroptosis is selectively activated in LDLR-driven myocarditis, and dimethyl fumarate treatment reduces cardiac inflammatory foci. • Human myocarditis autopsy hearts show up-regulated LDLR and ICAM-1, providing translational validation of the LDLR–OPN axis as a clinically relevant driver of inflammatory myocardial injury.
Keywords:
COVID-19
GSDMD
LDLR
myocarditis
OPN
SARS-CoV-2
chSARS-CoV-2
chimeric SARS-CoV-2
DMF
dimethyl fumarate
GSDMD
gasdermin D
IDOL
induced degrader of low-density lipoprotein receptor
ICAM-1
intercellular adhesion molecule-1
K18-hACE2tg
keratin 18 human angiotensin-converting enzyme 2 transgenic
LDLR
low-density lipoprotein receptor
MLKL
mixed lineage kinase domain-like protein
OPN
osteopontin
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