In recent years, autophagy, a metabolic, cytoplasmic quality control and general homeostatic process, has emerged as a central regulator of immune functions. So far, most of this evidence derives from immune cell-autonomous control of inflammation, with autophagy regulating the survival, differentiation, polarization and inflammatory mediator generation of diverse immune cell subsets. Crucially, our group has demonstrated that autophagy processes in endothelial cells, the portal governing the entry of leukocytes and macromolecules into tissues, are essential to limit neutrophil tissue recruitment during acute inflammation and associated tissue damage. However, the molecular mechanisms and nature of the autophagy processes regulating this phenomenon is still unknown. Hence, the main goal of our emerging laboratory is to decipher the molecular mechanisms through which endothelial cell autophagy pathways shape the inflammatory response with the aim of identifying new therapeutic approaches for the regulation of inflammatory disorders. Collectively, we aim to explore the initiating factors, molecular characteristics and pathophysiological relevance of endothelial autophagy processes during acute and chronic inflammation as well as ageing-associated pathologies.