Long-term cardiovascular complications following sepsis: is senescence the missing link?

With improved management of patients, sepsis survivors are increasing each year. Early cardiovascular complications, of yet undeciphered mechanisms, are an emerging health issue in post-sepsis syndrome. Premature senescence of endothelium and vascular tissue is proven an accelerated process of atherogenesis in young septic rats. An increasing body of clinical evidence point at endothelial senescence in the initiation and development of atherosclerosis. Prevention of premature senescence by senotherapy and cardiological follow-up could improve long-term septic patients’ outcomes. Among the long-term consequences of sepsis (also termed “post-sepsis syndrome”) the increased risk of unexplained cardiovascular complications, such as myocardial infarction, acute heart failure or stroke, is one of the emerging specific health concerns. The vascular accelerated ageing also named premature senescence is a potential mechanism contributing to atherothrombosis, consequently leading to cardiovascular events. Indeed, vascular senescence-associated major adverse cardiovascular events (MACE) are a potential feature in sepsis survivors and of the elderly at cardiovascular risk. In these patients, accelerated vascular senescence could be one of the potential facilitating mechanisms. This review will focus on premature senescence in sepsis regardless of age. It will highlight and refine the potential relationships between sepsis and accelerated vascular senescence. In particular, key cellular mechanisms contributing to cardiovascular events in post-sepsis syndrome will be highlighted, and potential therapeutic strategies to reduce the cardiovascular risk will be further discussed.