Roles of focal adhesion proteins in obesity related metabolic syndrome

This review explores the roles of focal adhesion (FA) proteins in obesity-related metabolic syndrome, focusing on their involvement in adipocyte function, insulin resistance, liver diseases, cardiovascular disorders, and aging. The aim is to synthesize current knowledge on how FA proteins contribute to metabolic dysregulation and identify potential therapeutic targets.

We conducted a comprehensive literature review of studies investigating FA proteins, including integrins, focal adhesion kinase (FAK), kindlin, and integrin-linked kinase (ILK), in obesity and related metabolic disorders. Data from transgenic mouse models, clinical studies, and molecular analyses were evaluated to elucidate the mechanisms by which FA proteins influence metabolic homeostasis.

FA proteins are critical regulators of cell-matrix interactions and mechanotransduction, impacting adipocyte differentiation, insulin sensitivity, and tissue remodeling. Dysregulation of these proteins is linked to metabolic disturbances, such as impaired adipocyte expansion, hepatic fibrosis, and cardiovascular dysfunction. For example, adipose-specific deletion of FAK or ILK alters insulin sensitivity, while integrin variants affect liver and muscle metabolism. Clinical evidence further supports the association of FA protein dysregulation with human diseases, including atherosclerosis and non-alcoholic fatty liver disease (NAFLD).

Targeting FA protein signaling pathways offers novel therapeutic opportunities for mitigating obesity-related metabolic syndrome. Understanding the molecular mechanisms of FA proteins in metabolic regulation could lead to innovative interventions to address the global burden of obesity and its complications. This review highlights the potential of FA proteins as biomarkers and therapeutic targets in metabolic diseases.