Atherosclerosis, the growth of fatty lesions in blood vessel walls, is the primary cause of human mortality. While many approaches have been demonstrated to slow its progression in mouse models, very few have been shown to reduce the size of established lesions. In a recent study, researchers found that a small molecule capable of increasing autophagy slowed the development of lesions in APOE-knockout mice. Autophagy is important in resisting stresses that contribute to atherosclerosis, making it a potential target for therapy. This study provides evidence that upregulating autophagy can slow the onset of atherosclerosis, offering hope for future treatments.
The study, titled “3,4-dimethoxychalcone induces autophagy and reduces neointimal hyperplasia and aortic lesions in mouse models of atherosclerosis,” also discusses the potential of other autophagy inducers in preventing cardiovascular diseases. The authors highlight the importance of identifying strategies to induce autophagy in all relevant cell types, such as cardiomyocytes, endothelial cells, and macrophages. Their findings suggest that 3,4-DC, a broad autophagy inducer, can efficiently slow the onset of atherosclerosis in mouse models. This research opens new possibilities for the development of therapies targeting autophagy to combat atherosclerosis.
