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Claudin Proteins: Their Potential Role in Obesity and Adipose Tissue Signaling, Physiology and Disease
Pablo Fernández-García1, Francesc Villarroya2,3, David Sánchez-Infantes1,2
1Area of Biochemistry and Molecular Biology and Genetics, Department of Basic Health Sciences, Campus Alcorcón, Rey Juan Carlos University (URJC), 28922 Alcorcón, Spain.
Abstract:
Obesity is one of the most challenging metabolic disorders affecting more than 800 million people around the world, according to the World Health Organization (WHO). In recent years, our knowledge and understanding of this multifactorial disease have been exponentially increasing, and many studies have been focusing on one of the main organs affected by obesity: adipose tissue (AT). It is known that AT undergoes remodeling due to the abnormal fat accumulation that accompanies obesity, characterized by increased immune cell infiltration, extracellular matrix (ECM) overproduction, and decreased adipogenesis, among others. Few studies have focused on adipocyte intercommunication, even though it is essential for AT homeostasis and function. In this context, GAP junction, adherens junction, and tight junction proteins can be found in these depots. In some cases, their function is well established, but in most cases it remains unknown. Claudins are the main proteins that form tight junctions (TJs), and, in recent years, studies have revealed a more extensive role of claudin proteins in intracellular signaling and control of a wide set of biological processes. This review aims to gather the main scientific evidence on the role of claudins in cell signaling, as well as what is known about these proteins in the field of obesity and adipose tissue physiology.
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