Research Progress on the Association Between Sarcopenic Obesity and Atherosclerosis: Current Status and Challenges.

Sarcopenic obesity (SO) is a syndrome characterized by a gradual reduction in skeletal muscle mass, strength, and function coupled with excessive fat accumulation, which considerably increases the risk of metabolic disorders and atherosclerotic cardiovascular disease. Owing to its extensive influence on the health of elderly individuals and distinct pathophysiological mechanisms, SO should be considered an independent clinical condition. Atherosclerosis, the fundamental pathophysiological underpinning of atherosclerotic cardiovascular disease, has garnered increased interest because of its association with SO. Existing research indicates that SO may synergistically promote atherosclerosis development through multiple pathways, including hormonal dysregulation, adipo-myokine imbalance, insulin resistance, chronic low-grade inflammation, and lipid metabolic abnormalities. The current literature gaps predominantly encompass the absence of standardized diagnostic criteria for SO, inconsistent results in studies investigating the relationship between SO and atherosclerosis, and inadequate causal validation. Studies indicate associations between SO and carotid atherosclerosis, coronary atherosclerosis, arterial stiffness, and 10-year atherosclerotic cardiovascular disease risk; however, conclusions remain inconsistent, and most studies are cross-sectional. Additionally, this field has insufficient focus on peripheral atherosclerosis, such as in the lower extremities. Moreover, the pathophysiological mechanisms remain unclear. A complex vicious cycle potentially exists among decreased muscle mass and function, fat accumulation, and atherosclerosis, a relationship that has not received sufficient attention. Therefore, this review aims to integrate existing evidence, summarize advances in diagnostic criteria for SO, review the epidemiological association between sarcopenic obesity and atherosclerosis, and analyze the reasons for heterogeneity in conclusions. It further explores potential pathophysiological mechanisms, delving into the vicious cycle among declining muscle mass and function, fat accumulation, and atherosclerosis. Finally, this review proposes future research directions, including diagnostic standardization, in-depth mechanism exploration, conducting prospective cohort studies to validate causal relationships, and developing intervention targets for SO-Atherosclerosis comorbidity.