The well-known condition of heart failure is a clinical syndrome that results when themyocardium's ability to pump enough blood to meet the body's metabolic needs isimpaired. Most of the cardiac activity is maintained by adrenoceptors, are categorizedinto two mainαandβand three distinct subtypes ofβreceptor:β1-,β2-, andβ3-adrenoceptors. Theβadrenoreceptor is the main regulatory macro proteins, pre-dominantly available on heart and responsible for down regulatory cardiac signaling.Moreover, the pathological involvement of Angiotensin-converting enzyme1 (ACE1)/angiotensin II (Ang II)/angiotensin II type 1 (AT1) axis and beneficial ACE2/Ang (1-7)/Mas receptor axis also shows protective role via Giβγ, during heart failurethese receptors get desensitized or internalized due to increase in the activity of G-protein-coupled receptor kinase 2 (GRK2) and GRK5, responsible for phosphorylationof G-protein-mediated down regulatory signaling. Here, we investigate the variousclinical and preclinical data that exhibit the molecular mechanism of upset level ofGRK change the cardiac activity during failing heart.
- G-protein-coupled receptors
- GPCR kinases
- beta adrenoreceptor
- chronic heart failure
- extracellular receptor kinase1/2
- mitogen-activated protein kinase
- renin-angiotensin-aldosterone system