ArticleAmerican journal of physiology. Heart and circulatory physiology2013
The β-arrestin-biased ligand TRV120023 inhibits angiotensin II-induced cardiac hypertrophy while preserving enhanced myofilament response to calcium.
Article in American journal of physiology. Heart and circulatory physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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44 citing papers in PubMed, 77 citations in OpenAlex.
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- Biased Allosteric Modulation in GPCR Drug Discovery.Handbook of experimental pharmacology · 2026Review
- G Protein-Coupled Receptors: A Century of Research and Discovery.Circulation research · 2024Review
- Myosin Light Chain Phosphatase Plays an Important Role in Cardiac Fibrosis in a Model of Mineralocorticoid Receptor-Associated Hypertension.Journal of the American Heart Association · 2024Article
- Insights Into the Role of Angiotensin-II ATHypertension (Dallas, Tex. : 1979) · 2024Review
- Review
- Pathophysiology and pharmacology of G protein-coupled receptors in the heart.Cardiovascular research · 2023Review
- Enhanced Bystander BRET (ebBRET) Biosensors as Biophysical Tools to Map the Signaling Profile of Neuropsychiatric Drugs Targeting GPCRs.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Molecular Effects of Auto-Antibodies on Angiotensin II Type 1 Receptor Signaling and Cell Proliferation.International journal of molecular sciences · 2022Article
- Identification and characterization of an atypical Gαs-biased βProceedings of the National Academy of Sciences of the United States of America · 2021Article
- β-Arrestin-Mediated Angiotensin II Type 1 Receptor Activation Promotes Pulmonary Vascular Remodeling in Pulmonary Hypertension.JACC. Basic to translational science · 2021Article
- Targeting the Angiotensin II Type 1 Receptor in Cerebrovascular Diseases: Biased Signaling Raises New Hopes.International journal of molecular sciences · 2021Review
- Beta-Arrestins in the Treatment of Heart Failure Related to Hypertension: A Comprehensive Review.Pharmaceutics · 2021Review
- GRK2 mediates β-arrestin interactions with 5-HTJournal of virology · 2021Article
- The Mechanism of Ajmaline and Thus Brugada Syndrome: Not Only the Sodium Channel!Frontiers in cardiovascular medicine · 2021Review
- B-arrestin-2 Signaling Is Important to Preserve Cardiac Function During Aging.Frontiers in physiology · 2021Article
- Stretch-Induced Biased Signaling in Angiotensin II Type 1 and Apelin Receptors for the Mediation of Cardiac Contractility and Hypertrophy.Frontiers in physiology · 2020Review
- Novel high molecular weight albumin-conjugated angiotensin II activates β-arrestin and G-protein pathways.Endocrine · 2019Article
- Therapeutic Potential of Targeting ß-Arrestin.Frontiers in pharmacology · 2019Review
- Biased agonists of the chemokine receptor CXCR3 differentially control chemotaxis and inflammation.Science signaling · 2018Article
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Authors and funding
8 authors at 2 institutions in 1 country.
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Abstract
In the present study, we compared the cardioprotective effects of TRV120023, a novel angiotensin II (ANG II) type 1 receptor (AT1R) ligand, which blocks G protein coupling but stimulates β-arrestin signaling, against treatment with losartan, a conventional AT1R blocker in the treatment of cardiac hypertrophy and regulation of myofilament activity and phosphorylation. Rats were subjected to 3 wk of treatment with saline, ANG II, ANG II + losartan, ANG II + TRV120023, or TRV120023 alone. ANG II induced increased left ventricular mass compared with rats that received ANG II + losartan or ANG II + TRV120023. Compared with saline controls, ANG II induced a significant increase in pCa50 and maximum Ca(2+)-activated myofilament tension but reduced the Hill coefficient (nH). TRV120023 increased maximum tension and pCa50, although to lesser extent than ANG II. In contrast to ANG II, TRV120023 increased nH. Losartan blocked the effects of ANG II on pCa50 and nH and reduced maximum tension below that of saline controls. ANG II + TRV120023 showed responses similar to those of TRV120023 alone; compared with ANG II + losartan, ANG II + TRV120023 preserved maximum tension and increased both pCa50 and cooperativity. Tropomyosin phosphorylation was lower in myofilaments from saline-treated hearts compared with the other groups. Phosphorylation of cardiac troponin I was significantly reduced in ANG II + TRV120023 and TRV120023 groups versus saline controls, and myosin-binding protein C phosphorylation at Ser(282) was unaffected by ANG II or losartan but significantly reduced with TRV120023 treatment compared with all other groups. Our data indicate that TRV120023-related promotion of β-arrestin signaling and enhanced contractility involves a mechanism promoting the myofilament response to Ca(2+) via altered protein phosphorylation. Selective activation of β-arrestin-dependent pathways may provide advantages over conventional AT1R blockers.
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