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

Altamish, M; Samuel, VP; Dahiya, R; Singh, Y; Deb, PK; Bakshi, HA; Tambuwala, MM; Chellappan, DK; Collet, T; Dua, K; Gupta, G

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

Altamish, M Samuel, VP Dahiya, R Singh, Y Deb, PK Bakshi, HA Tambuwala, MM Chellappan, DK Collet, T Dua, K

Gupta, G

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Publisher:: Wiley
Publication Type:: Journal Article
Citation:: Drug Development Research, 2020, 81, (1), pp. 23-31
Issue Date:: 2020

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Field	Value	Language
dc.contributor.author	Altamish, M
dc.contributor.author	Samuel, VP
dc.contributor.author	Dahiya, R
dc.contributor.author	Singh, Y
dc.contributor.author	Deb, PK
dc.contributor.author	Bakshi, HA
dc.contributor.author	Tambuwala, MM
dc.contributor.author	Chellappan, DK
dc.contributor.author	Collet, T
dc.contributor.author	Dua, K https://orcid.org/0000-0002-7507-1159
dc.contributor.author	Gupta, G
dc.date.accessioned	2020-08-24T05:45:23Z
dc.date.available	2019-11-13
dc.date.available	2020-08-24T05:45:23Z
dc.date.issued	2020
dc.identifier.citation	Drug Development Research, 2020, 81, (1), pp. 23-31
dc.identifier.issn	0272-4391
dc.identifier.issn	1098-2299
dc.identifier.uri	http://hdl.handle.net/10453/142327
dc.description.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.
dc.format	Print-Electronic
dc.language	eng
dc.publisher	Wiley
dc.relation.ispartof	Drug Development Research
dc.relation.isbasedon	10.1002/ddr.21627
dc.rights	info:eu-repo/semantics/closedAccess
dc.subject	1115 Pharmacology and Pharmaceutical Sciences
dc.subject.classification	Pharmacology & Pharmacy
dc.title	Molecular signaling of G-protein-coupled receptor in chronic heart failure and associated complications.
dc.type	Journal Article
utslib.citation.volume	81
utslib.location.activity	United States
utslib.for	1115 Pharmacology and Pharmaceutical Sciences
utslib.for	1115 Pharmacology and Pharmaceutical Sciences
pubs.organisational-group	/University of Technology Sydney/Faculty of Health
pubs.organisational-group	/University of Technology Sydney/Faculty of Health/Graduate School of Health/GSH.Pharmacy
pubs.organisational-group	/University of Technology Sydney
pubs.organisational-group	/University of Technology Sydney/Faculty of Health/Graduate School of Health
utslib.copyright.status	closed_access	*
pubs.consider-herdc	true
dc.date.updated	2020-08-24T05:45:18Z
pubs.issue	1
pubs.publication-status	Published online
pubs.volume	81
utslib.citation.issue	1

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.

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http://hdl.handle.net/10453/142327