The Role of Galectin-3 in Atherosclerosis and Its Cardiovascular Complications: An Update

Atherosclerosis is a primary cause of vascular disease worldwide, resulting in diverse clinical manifestations that contribute to significant morbidity and mortality. It is widely recognized as a multifactorial condition involving both metabolic and oxidative mechanisms. The initiation of atherosclerotic plaques arises from endothelial injury caused by excess lipid-carrying lipoproteins, which trigger an exaggerated pro-inflammatory response. This response is mediated by proteins such as galectin-3 (Gal-3), secreted by monocytes and macrophages, which stimulate and accelerate plaque formation. Because of its largely asymptomatic progression, atherosclerosis remains difficult to diagnose. In recent years, clinical and preclinical research on Gal-3 has expanded considerably, revealing elevated Gal-3 levels in patients with atheroma. Moreover, preclinical studies demonstrate that Gal-3 inhibition or gene suppression can effectively attenuate the development of atherosclerosis. These findings highlight the involvement of monocytes, macrophages, foam cells, and Gal-3 in the initiation and progression of the disease. Consequently, Gal-3 has emerged as a promising biomarker for endothelial dysfunction and other cardiovascular conditions. This review therefore summarizes current evidence on the role of Gal-3 in the pathogenesis, clinical features, diagnosis, treatment, and prognosis of atherosclerosis, while also encouraging discussion of Gal-3 as a potential therapeutic strategy.