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.
Disclosure of Potential Conflicts of Interest
No potential conflict of interest was disclosed.
Acknowledgments
This manuscript was prepared under the scope of Grants funded by the European Foundation for the Study of Diabetes (EFSD)/ Glaxo Smith Kline (GSK) Programme and the Foundation for Science and Technology (PEst-C/SAU/UI3282/2011 and COMPETE-FEDER).