Researchers have discovered that a long non-coding RNA called NORAD plays a crucial role in maintaining the health of endothelial cells, which line the blood vessels. By acting as a “sponge” to regulate other molecules, NORAD helps prevent a harmful process called ferroptosis that can damage these cells and contribute to the development of atherosclerosis. This finding could lead to new therapies for heart and cardiovascular diseases.
Keeping the cells that line our blood vessels healthy is essential for maintaining a strong and flexible cardiovascular system. When these endothelial cells become damaged or dysfunctional, it can set off a chain of events that ultimately leads to the buildup of plaque in the arteries – a condition known as atherosclerosis. This narrowing of the blood vessels increases the risk of heart attacks, strokes, and other serious cardiovascular problems.
Uncovering a Master Regulator of Endothelial Cell Health
In a recent study, researchers have identified a long non-coding RNA (lncRNA) called NORAD as a key player in maintaining the health and function of endothelial cells. LncRNAs are molecules that don’t code for proteins but instead play important regulatory roles in the cell.
The team found that levels of NORAD were significantly elevated in the blood of patients with coronary artery disease (CAD) compared to healthy individuals. Further investigation revealed that NORAD acts as a “sponge,” binding to and sequestering other molecules called microRNAs that would otherwise interfere with the expression of important genes involved in cell growth and survival.
NORAD Protects Cells from Ferroptosis
One of the key genes regulated by NORAD is CCND1, which codes for a protein called cyclin D1 that plays a crucial role in controlling the cell cycle. By preventing the degradation of cyclin D1, NORAD helps endothelial cells proliferate and migrate properly.
But NORAD’s protective effects go beyond just regulating the cell cycle. The researchers also found that knocking down NORAD in endothelial cells led to a increase in oxidative stress and the activation of a form of regulated cell death called ferroptosis.
Ferroptosis is characterized by the buildup of toxic lipid peroxides and the depletion of antioxidants like glutathione. This can ultimately cause the cell membrane to rupture and the cell to die. By maintaining the expression of key ferroptosis-regulating proteins like GPX4 and FTH1, NORAD appears to shield endothelial cells from this destructive process.
Implications for Cardiovascular Health
The findings from this study suggest that NORAD could be a valuable target for new therapies aimed at preventing or treating cardiovascular diseases like atherosclerosis. By preserving the health and function of endothelial cells, boosting NORAD levels or activity could potentially slow the progression of plaque buildup in the arteries.
Additionally, the researchers noted that NORAD levels in the blood could serve as a useful biomarker for identifying individuals at high risk of developing CAD. Further studies will be needed to fully understand how NORAD exerts its protective effects and explore its potential as a diagnostic and therapeutic tool.
Overall, this research highlights the crucial role that regulatory RNAs like NORAD can play in maintaining the delicate balance of processes that keep our cardiovascular system functioning properly. By uncovering these molecular mechanisms, scientists are getting closer to developing more targeted and effective ways to combat heart and vascular diseases.
Author credit: This article is based on research by Tao He, Junxing Pu, Haijing Ge, Tianli Liu, Xintong Lv, Yu Zhang, Jia Cao, Hong Yu, Zhibing Lu, Fen Du.
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