Abstract
After menopause, the incidence of cardiovascular disease in women rises sharply, especially coronary artery disease (CAD), which has become a major health concern for women worldwide. Previous perspectives have held that decreased estrogen levels are the main cause of the elevated risk among postmenopausal women. In recent years, increasing evidence has suggested that follicle-stimulating hormone (FSH), whose levels surge postmenopausally, may play a pivotal role in this process. This review aims to systematically summarize current evidence from clinical and animal studies to evaluate the relationship between FSH and CAD risk in postmenopausal women, exploring the conflicting evidence and examining its potential effects in both the pathogenesis of atherosclerosis and the regulation of cardiometabolic risk factors. It has been confirmed by multiple studies that elevated FSH, by engaging follicle-stimulating hormone receptor (FSHR) in the liver and inflammatory cells, disrupts lipid metabolism and exacerbates vascular inflammation, thereby promoting the progression of CAD. Epidemiological evidence also supports this point. However, some clinical studies show contrasting evidence, indicating that FSH might exert a protective effect in certain contexts, possibly by influencing various metabolic pathways. In conclusion, there is increasing evidence suggesting that FSH levels play a role in the development of CAD in postmenopausal women, yet the current body of evidence is characterized by predominantly observational study designs and inconsistent findings. Therefore, it is particularly important for future research to further verify this association and clarify the causal relationship. By synthesizing the proposed mechanistic pathways, this review highlights implications for future research, which can explore the potential of FSH and FSHR as biomarkers and therapeutic targets for coronary atherosclerosis risk stratification, assessment, and intervention in this postmenopausal population.