2024
DOI: 10.1161/hypertensionaha.123.19419
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Insights Into the Role of Angiotensin-II AT 1 Receptor-Dependent β-Arrestin Signaling in Cardiovascular Disease

Abstract: β-arrestins are a family of intracellular signaling proteins that play a key role in regulating the activity of G protein-coupled receptors. The angiotensin-II type 1 receptor is an important G protein-coupled receptor involved in the regulation of cardiovascular function and has been implicated in the progression of cardiovascular diseases. In addition to canonical G protein signaling, G protein-coupled receptors including the angiotensin-II type 1 receptor can signal via β-arrestin. Dysregulation of β-arrest… Show more

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Cited by 5 publications
(2 citation statements)
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“…19,20 There is also evidence supporting a noncanonical signaling role for ARRB downstream of AT 1 R. [21][22][23] Indeed, activation of this noncanonical pathway has gained a lot of attention as it has been shown to counterbalance maladaptive G-protein signaling during disease. 24 Our prior work showed that central activation of the AT 1 R ARRB axis using the biased ligand TRV120027 (TRV027) lowered BP and reduced 0.15 mol/L saline intake during DOCA-salt treatment. 25 Furthermore, we demonstrated that global genetic deletion of ARRB2 (β-arrestin 2) resulted in higher saline intake and an exacerbated pressor response to DOCA-salt treatment.…”
Section: Clinical/pathophysiological Implicationsmentioning
confidence: 99%
“…19,20 There is also evidence supporting a noncanonical signaling role for ARRB downstream of AT 1 R. [21][22][23] Indeed, activation of this noncanonical pathway has gained a lot of attention as it has been shown to counterbalance maladaptive G-protein signaling during disease. 24 Our prior work showed that central activation of the AT 1 R ARRB axis using the biased ligand TRV120027 (TRV027) lowered BP and reduced 0.15 mol/L saline intake during DOCA-salt treatment. 25 Furthermore, we demonstrated that global genetic deletion of ARRB2 (β-arrestin 2) resulted in higher saline intake and an exacerbated pressor response to DOCA-salt treatment.…”
Section: Clinical/pathophysiological Implicationsmentioning
confidence: 99%
“…51 Data from our group have shown that TRV027, a β-arrestin-biased AT 1 R ligand, did not reduce ACE2 activity and expression, in contrast to Ang-II administration. 52 Noteworthy, TRV027 did not pass a 30-day phase IIB clinical trial, 53,54 but in vivo results showed beneficial effects in the treatment of cardiac failure, acute respiratory distress syndrome, and abnormal clotting, suggesting that a derivative compound could show clinical efficacy.…”
Section: Ace2mentioning
confidence: 99%