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Macrophage-Specific SPP1 Contributes to Pressure Overload–Induced Cardiac Dysfunction and Maladaptive Remodeling
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DOI：10.1016/j.jacbts.2026.101623.png)
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Abstract
En 中文
• A novel SPP1+ macrophage emerges early in pressure overload-driven cardiac remodeling. • Myeloid-specific Spp1 deletion alleviates pressure overload-induced cardiac inflammation, remodeling and dysfunction. • The HMGB1-NLRP3-NF-κB axis in macrophages drives pathogenic SPP1 production. • Arglabin, a selective NLRP3 inhibitor, suppresses SPP1 and thereby confers cardioprotection under pressure overload.
Keywords:
arglabin
cardiac remodeling
macrophage
pressure overload
SPP1
AMCF
adult mouse cardiac fibroblast
ARG
arglabin
CCR2
C-C chemokine receptor 2
DCM
dilated cardiomyopathy
DEG
differentially expressed gene
ECM
extracellular matrix
EF
ejection fraction
FS
fractional shortening
HF
heart failure
HFpEF
heart failure with preserved ejection fraction
HMGB1
high-mobility group box 1
HW/BW
heart weight–to–body weight ratio
LV
left ventricular
LVIDs
left ventricular internal dimension at end-systole
LVPWd
left ventricular posterior wall thickness at end-diastole
NMCM
neonatal mouse cardiomyocyte
PM
peritoneal macrophage
PO
pressure overload
scRNA-seq
single-cell RNA sequencing
SPP1
secreted phosphoprotein 1
Spp1f/f
LoxP-flanked Spp1
Spp1MyeKO
myeloid-specific Spp1-knockout
TAC
transverse aortic constriction
Journal
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