The internalization of angiotensin II type 1 receptor (ATR) plays an important role in maintaining cardiovascular homeostasis. Decreased receptor internalization is closely related to cardiovascular diseases induced by the abnormal activation of ATR, such as hypertension. However, the mechanism behind reduced ATR internalization is not fully understood. This review focuses on four parts of the receptor internalization process (the combination of agonists and receptors, receptor phosphorylation, endocytosis, and recycling) and summarizes the possible mechanisms by which ATR internalization is reduced based on these four parts of the process. (1) The agonist has a large molecular weight or a stronger ability to hydrolyze phosphatidylinositol 4,5-bisphosphate (PtdIns (4,5) P), which can increase the consumption of PtdIns (4,5) P. (2) ATR phosphorylation is weakened because of an abnormal function of phosphorylated kinase or changes in phospho-barcoding and GPCR-β-arrestin complex conformation. (3) The abnormal formation of vesicles or ATR heterodimers with fewer endocytic receptors results in less ATR endocytosis. (4) The enhanced activity and upregulated expression of small GTP-binding protein 4 (Rab4) and 11 (Rab11), which regulate receptor recycling, and phosphatidylinositol 3-kinase increase ATR recycling. In addition, lower expression of ATR-associated protein (ATRAP) or higher expression of ATR-associated protein 1 (ARAP1) can reduce receptor internalization.
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