G protein-coupled receptor kinase 2 (GRK2) is emerging as a pivotal signalling hub able to integrate different transduction cascades. This ability appears to underlie its central role in different physiological and pathological conditions. Key mediators of cardiovascular function (such as catecholamines or angiotensin II) and components of the systemic milieu altered in insulin resistance conditions converge in increasing GRK2 levels in diverse cardiovascular cell types. In turn, GRK2 would simultaneously modulate several cardiovascular regulatory pathways, including GPCR and insulin signalling cascades, NO bioavailability and mitochondrial function. This fact can help explain the contribution of increased GRK2 levels to maladaptive cardiovascular function and remodeling. It also unveils GRK2 as a link between cardiovascular pathologies and co-morbidities such as obesity or type 2 diabetes. On the other hand, enhanced GRK2 expression, as observed in adipose tissues, liver or skeletal muscle during insulin resistance-related pathologies, could modify the orchestration of GPCR and insulin signalling in these crucial metabolic organs, and contribute to key features of the obese and insulin-resistant phenotype.

G蛋白偶联受体激酶2（GRK2）作为能够整合不同转导级联反应的关键信号枢纽而出现。这种能力似乎是其在不同生理和病理条件下的核心作用的基础。心血管功能的关键介体（例如儿茶酚胺或血管紧张素II）和胰岛素抵抗条件中改变的全身环境成分在多种心血管细胞类型中的GRK2水平升高中趋同。反过来，GRK2将同时调节几种心血管调节途径，包括GPCR和胰岛素信号传导级联，NO生物利用度和线粒体功能。这一事实可以帮助解释GRK2水平升高对适应不良的心血管功能和重塑的作用。它还揭示了GRK2，将其作为心血管疾病与合并症（例如肥胖症或2型糖尿病）之间的联系。另一方面，在胰岛素抵抗相关的病理过程中，在脂肪组织，肝脏或骨骼肌中观察到GRK2表达增强，