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Rheumatic Heart Disease
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DOI：10.1016/j.jacbts.2026.101629.png)
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Abstract
En 中文
• RHD causes premature cardiovascular morbidity without disease-modifying therapy. • This review links immune, inflammation, mechanical, and fibrotic pathways in RHD valves. • SGLT2 inhibitors may target key pathways but need RHD-specific validation. • Future studies should prioritize valve tissue, relevant models, and trials.
Keywords:
endothelial dysfunction
rheumatic heart disease
SGLT2 inhibitors
valve remodeling
valvular chronic inflammation
ARF
acute rheumatic fever
AS
aortic stenosis
CAVD
calcific aortic valve disease
ECM
extracellular matrix
EndMT
endothelial-to-mesenchymal transition
eNOS
endothelial nitric oxide synthase
GAS
group A Streptococcus
GlcNAc
N-acetylglucosamine
IL
interleukin
LMICs
low- and middle-income countries
LYVE-1
lymphatic vessel endothelial hyaluronan receptor 1
miRNA
microRNA
MMP
matrix metalloproteinase
MR
mitral regurgitation
mVEC
mitral valve endothelial cell
mVIC
mitral valve interstitial cell
RHD
rheumatic heart disease
SGLT2i
sodium-glucose cotransporter 2 inhibitor
TGF
transforming growth factor
TIMP
tissue inhibitor of metalloproteinase
TLR2
Toll-like receptor 2
TNF
tumor necrosis factor
VCAM
vascular cell adhesion molecule
VEGF
vascular endothelial growth factor
VIC
valvular interstitial cell
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