TY - JOUR
T1 - Molecular signaling of G‐protein‐coupled receptor in chronic heart failure and associated complications
AU - Altamish, Mohammad
AU - Samuel, Vijaya Paul
AU - Dahiya, Rajiv
AU - Singh, Yogendra
AU - Deb, Pran Kishore
AU - Bakshi, Hamid A.
AU - Tambuwala, Murtaza M.
AU - Chellappan, Dinesh K.
AU - Collet, Trudi
AU - Dua, Kamal
AU - Gupta, Gaurav
PY - 2019/11/30
Y1 - 2019/11/30
N2 - 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.
AB - 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.
KW - G-protein-coupled receptors
KW - GPCR kinases
KW - beta adrenoreceptor
KW - chronic heart failure
KW - extracellular receptor kinase1/2
KW - mitogen-activated protein kinase
KW - renin-angiotensin-aldosterone system
UR - http://www.scopus.com/inward/record.url?scp=85075799271&partnerID=8YFLogxK
U2 - 10.1002/ddr.21627
DO - 10.1002/ddr.21627
M3 - Article
C2 - 31785110
SN - 0272-4391
JO - Drug Development Research
JF - Drug Development Research
ER -
