Abstract
Claudins are pivotal building blocks of tight junctions that form the paracellular barrier in epithelia and endothelia. In mammals, claudins are a 27-gene family that encodes tetraspan membrane proteins, playing a crucial role in the formation and integrity of tight junctions and regulate the barrier function. Claudin isoforms are expressed in a tissue- and/or developmental stage-dependent manner. A growing body of evidence indicates that pathological states characterized by neuroinflammation, such as Alzheimer disease, multiple sclerosis, diabetic retinopathy and retinopathy of prematurity share a common feature: the barrier breakdown. This review aims integrating and summarizing the most relevant and recent work developed in the field of claudins, with particular attention to their role in blood-brain and blood-retinal barriers, as well as describing their regulation in the aforementioned human diseases.