Molecular signaling of G‐protein‐coupled receptor in chronic heart failure and associated complications

Abstract

The well‐known condition of heart failure is a clinical syndrome that results when the myocardium's ability to pump enough blood to meet the body's metabolic needs is impaired. Most of the cardiac activity is maintained by adrenoceptors, are categorized into two main α and β and three distinct subtypes of β receptor: β1‐, β2‐, and β3‐adrenoceptors. The β adrenoreceptor is the main regulatory macro proteins, predominantly available on heart and responsible for down regulatory cardiac signaling. Moreover, the pathological involvement of Angiotensin‐converting enzyme 1 (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 Gi βγ, during heart failure these receptors get desensitized or internalized due to increase in the activity of G‐protein‐coupled receptor kinase 2 (GRK2) and GRK5, responsible for phosphorylation of G‐protein‐mediated down regulatory signaling. Here, we investigate the various clinical and preclinical data that exhibit the molecular mechanism of upset level of GRK change the cardiac activity during failing heart.

Effects of enteral nutrition on heart function, inflammatory markers and immune function in elderly patients with chronic heart failure

“… 20 The deficiency of protein can directly lead to the contractile function of cardiomyocytes and accelerate their death. 21 In view of this, a more individualized nutritional therapy is preferred for patients with CHF.…”

Call for Papers for a Virtual Special Issue on GPCR Signaling

“…The full extent of this phenomenon and its physiological ramifications remain to be fully elucidated. In this context, it is now thought that the AT1 receptor may be internalized by G protein-independent signals through mechanisms actually mediated by β-arrestin and GRKs . Modulating the GRK (and arrestin) functions in these cases could serve to increase myocardial responsiveness.…”

Relationship between G protein level with left ventricular systolic function in children with acyanotic heart disease

“…When the β and γ chains come together, they form a potent βγ complex, anchoring the G protein firmly to the cytoplasmic surface of the plasma membrane [16,17]. Most cardiac activity is managed by adrenoreceptors, consisting of two central receptors, α and β. Adrenoreceptors β are the main regulatory macro-proteins, predominantly found in the heart and are responsible for lowering cardiac signals [18,19]. Heart failure patients often exhibit elevated levels of circulated adenylate cyclase, resulting in hyperstimulation of adrenergic receptors and increased presence of G-protein-coupled receptor kinase (GRK) in the heart [16,19].…”

“…Most cardiac activity is managed by adrenoreceptors, consisting of two central receptors, α and β. Adrenoreceptors β are the main regulatory macro-proteins, predominantly found in the heart and are responsible for lowering cardiac signals [18,19]. Heart failure patients often exhibit elevated levels of circulated adenylate cyclase, resulting in hyperstimulation of adrenergic receptors and increased presence of G-protein-coupled receptor kinase (GRK) in the heart [16,19]. Research on G proteins in children with heart failure remains limited, with scarce attention directed towards this demographic.…”