Table 2.

Animal models of GRKs genetic modifications affecting cardiac functions.

GRK studied	Animal model	Main findings	Reference
GRK2	GRK2 -/- KO mice	Embryonic lethality	Matkovich et al., 2006
	GRK2+/- mice	Enhanced expression of key genes involved in physiological hypertrophy/cardioprotection Enhanced cardiac insulin sensitivity	Lucas et al., 2014
	GRK2 cardiac overexpression	Decreased β-adrenergic (β-AR) signaling (Attenuation of contractility and heart rate in response to a β-agonist) Desensitized AT1 receptor (AT1R)-mediated responses to angiotensin II (Ang II)	Koch et al., 1995
	Transgenic mice with GRK2 vascular smooth muscle (VSM) targeted overexpression	Increased blood pressure levels Cardiac hypertrophy	Eckhart et al., 2002
GRK4	Mice carrying the naturally occurring polymorphism A142V in GRK4γ (polymorphism linked to hypertension in genetic studies)	Development of hypertension Impaired diuretic and natriuretic effects of dopamine D1 Receptor agonists	Felder et al., 2002
GRK5	Mice bearing targeted deletion of the GRK5 gene between exons 7 and 8 (GRK5-KO)	Muscarinic supersensitivity and impaired receptor desensitization	Gainetdinov et al., 1999
	Cardiac GRK5 overexpression	Decreased β-AR signaling (Attenuation of contractility and heart rate in response to a β-agonist) No effects on AT1R signaling in response to Ang II	Rockman et al., 1996

GRK, G protein-coupled receptor kinase.