Inflammation is at the basis of a plethora of diseases with very different aetiological origins. Although this immune reaction plays a paramount role during host survival and tissue repair, inflammation must be tightly regulated to avoid excessive tissue damage and the instigation of inflammatory diseases. For instance, uncontrolled recruitment of immune cells from blood vessels to injured tissues, as well as dysregulated vascular leakage, can lead to the development of numerous pathologies, including highly prevalent cardiovascular, metabolic and infectious conditions as well as tumour progression. Therefore, understanding the mechanisms through which the vasculature becomes dysfunctional during pathological inflammation is an area of extremely forefront research interest.

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.