Key result
SNHG3 silencing reduces aortic valve calcification in preclinical models by activating BMP2 expression.
Why the study?
SNHG3 was identified as a highly expressed lncRNA in calcific aortic valve disease, but its role in aortic valve calcification was not fully understood.
SNHG3 promotes aortic valve calcification by upregulating BMP2, identifying it as a potential novel therapeutic target for calcific aortic valve disease.
SNHG3 emerges as a candidate target in calcific aortic valve disease; leaves open translation from animal models to human therapy.
Based on high-throughput transcriptomic sequencing, SNHG3 was among the most highly expressed long noncoding RNAs in calcific aortic valve disease. SNHG3 upregulation was verified in human and mouse calcified aortic valves. Moreover, in vivo and in vitro studies showed SNHG3 silencing markedly ameliorated aortic valve calcification. In-depth functional assays showed SNHG3 physically interacted with polycomb repressive complex 2 to suppress the H3K27 trimethylation BMP2 locus, which in turn activated BMP2 expression and signaling pathways. Taken together, SNHG3 promoted aortic valve calcification by upregulating BMP2, which might be a novel therapeutic target in human calcific aortic valve disease.
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Chen et al. (2022) studied Calcific aortic valve disease. SNHG3 silencing was evaluated on Aortic valve calcification. SNHG3 silencing markedly ameliorated aortic valve calcification in vivo and in vitro by interacting with polycomb repressive complex 2 to activate BMP2 expression.
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