Key result
Increased ANRIL expression in acute coronary syndrome patients was associated with inflammatory cytokines, and its knockdown in vitro inhibited endothelial inflammatory activation and apoptosis.
Why the study?
Although lncRNA ANRIL plays a critical role in atherosclerosis development, its precise effect on endothelial dysfunction remained unclear.
Observational (n=111)
ANRIL regulates endothelial dysfunction via the let-7b/TGF-βR1/Smad pathway, highlighting a potential therapeutic target for cardiovascular disease.
Hypothesis-generating for ANRIL as an endothelial target in ACS; human studies needed before any clinical consideration.
The long noncoding RNA antisense noncoding RNA in the INK4 locus (ANRIL) plays a critical role in the development of atherosclerosis. However, the precise effect of ANRIL on endothelial dysfunction remains unclear. In this study, we investigated ANRIL expression in patients with coronary artery disease and elucidated the molecular mechanism underlying its effect. ANRIL expression was detected in the blood plasma of 111 patients. We analysed the correlation between ANRIL and endothelial dysfunction markers. We also examined the effect of ANRIL on the regulation of endothelial dysfunction. ANRIL levels were increased in patients with acute coronary syndrome. The expression of ANRIL is associated with the inflammatory cytokines monocyte chemoattractant protein-1 and interleukin-10, which are secreted in response to endothelial dysfunction. Knockdown of ANRIL significantly promoted cell proliferation and tubule formation and inhibited inflammatory activation and apoptosis of human umbilical vein endothelial cells (HUVEC). ANRIL-mediated inhibition of let-7b regulates HUVEC dysfunction by targeting the TGF-βR1/Smad signalling pathway. This study highlights a new therapeutic strategy for preventing endothelial dysfunction associated with cardiovascular disease.
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Liu et al. (2020) conducted an observational in Coronary artery disease (n=111). ANRIL expression was evaluated on Correlation between ANRIL and endothelial dysfunction markers. Increased ANRIL expression in acute coronary syndrome patients was associated with inflammatory cytokines, and its knockdown in vitro inhibited endothelial inflammatory activation and apoptosis.
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