TREM2 Influences the Formation of Unstable Atherosclerotic Plaque
The development of unstable atherosclerotic plaques in blood vessels can have detrimental effects on cardiovascular health, often leading to severe complications such as heart attacks and strokes. Understanding the factors that contribute to plaque instability is crucial in reducing cardiovascular mortality. Recent research has highlighted the role of the triggering receptor expressed on myeloid cells 2 (TREM2) in atherosclerosis. Studies have shown that TREM2 deficiency can increase necrotic core formation in early atherosclerosis, while TREM2 agonism can decrease it. Additionally, TREM2 plays a crucial role in the efferocytosis process of macrophages, influencing the balance between foam cell death and clearance in atherosclerotic lesions. This highlights the importance of TREM2 in controlling plaque necrosis and ultimately influencing the stability of atherosclerotic plaques.
Atherosclerosis, driven by lipid accumulation and inflammation in arterial walls, is a major cause of cardiovascular mortality globally. Understanding the functions of TREM2 in regulating myeloid cell activities in atherosclerosis is a key area of interest for researchers. The findings suggest that TREM2 has a significant impact on the progression and stability of atherosclerotic plaques, shedding light on potential therapeutic targets for cardiovascular diseases.
