Advances in the Mechanistic Research of Metabolic Syndrome and Stroke-Associated Pneumonia

Stroke-associated pneumonia (SAP) is a major cause of morbidity and mortality in stroke patients, ranking as the third leading cause of death. Emerging evidence suggests that metabolic syndrome (MetS) significantly contributes to the development and progression of SAP, acting through multiple pathways that exacerbate inflammation and adversely affect patient outcomes. This review delves into the intricate relationship between MetS and SAP, exploring potential mechanisms underlying this association based on current research findings. Insulin resistance and obesity, prevalent in stroke patients, are implicated in the exacerbation of chronic inflammation by promoting the secretion of pro-inflammatory cytokines, such as TNF-α. Furthermore, hypertension, a hallmark of MetS, can exacerbate pulmonary infections by over-activating the sympathetic nervous system. This activation triggers the renin-angiotensin-aldosterone system (RAAS), leading to the production of the pro-inflammatory mediator Ang II and the subsequent release of pro-inflammatory cytokines. Moreover, chronic inflammation, driven by the effects of pro-inflammatory cytokines and chronic stress responses, can perpetuate metabolic disturbances, creating a vicious cycle that further exacerbates the disease process. This review underscores the importance of addressing both metabolic dysregulation and other contributing factors to SAP, such as dysphagia, for effective clinical management of stroke patients. By targeting these interconnected pathways, clinicians can potentially break the vicious cycle, leading to improved outcomes for stroke patients.