ArticleJournal of the American Heart Association2018
Regulator of G Protein Signaling 6 Facilities Cardiac Hypertrophy by Activating Apoptosis Signal-Regulating Kinase 1-P38/c-JUN N-Terminal Kinase 1/2 Signaling.
Article in Journal of the American Heart Association, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 24 citations in OpenAlex.
- Discovery of ancestry-specific variants associated with clopidogrel response among Caribbean Hispanics.NPJ genomic medicine · 2025Article
- G protein regulation by RGS proteins in the pathophysiology of dilated cardiomyopathy.American journal of physiology. Heart and circulatory physiology · 2025Review
- Heart failure with preserved ejection fraction in pigs causes shifts in posttranscriptional checkpoints.American journal of physiology. Heart and circulatory physiology · 2024Article
- RGS proteins and cardiovascular Angiotensin II Signaling: Novel opportunities for therapeutic targeting.Biochemical pharmacology · 2023Review
- Discovery of Ancestry-specific Variants Associated with Clopidogrel Response among Caribbean Hispanics.medRxiv : the preprint server for health sciences · 2023Article
- Cryptotanshinone Attenuated Pathological Cardiac RemodelingOxidative medicine and cellular longevity · 2023Article
- The association between RGS4 and choline in cardiac fibrosis.Cell communication and signaling : CCS · 2021Article
- Dual-specificity Phosphatase 9 protects against Cardiac Hypertrophy by targeting ASK1.International journal of biological sciences · 2021Article
- The role of post-translational modifications in cardiac hypertrophy.Journal of cellular and molecular medicine · 2019Review
- Regulator of G Protein Signaling 6 Facilities Cardiac Hypertrophy by Activating Apoptosis Signal-Regulating Kinase 1-P38/c-JUN N-Terminal Kinase 1/2 Signaling.Journal of the American Heart Association · 2018Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background Regulator of G protein signaling 6 ( RGS 6) is an important member of the RGS family and produces pleiotropic regulatory effects on cardiac pathophysiology. However, the role of RGS 6 protein in cardiomyocytes during angiotensin II - and pressure overload-induced cardiac hypertrophy remain unknown. Methods and Results Here, we used a genetic approach to study the regulatory role of RGS 6 in cardiomyocytes during pathological cardiac hypertrophy. RGS 6 expression was significantly increased in failing human hearts and in hypertrophic murine hearts. The extent of aortic banding-induced cardiac hypertrophy, dysfunction, and fibrosis in cardiac-specific RGS 6 knockout mice was alleviated, whereas the hearts of transgenic mice with cardiac-specific RGS 6 overexpression exhibited exacerbated responses to pressure overload. Consistent with these findings, RGS 6 also facilitated an angiotensin II -induced hypertrophic response in isolated cardiomyocytes. According to the mechanistic studies, RGS 6 mediated cardiac hypertrophy by directly interacting with apoptosis signal-regulating kinase 1, which further activates the P38-c- JUN N-terminal kinase 1/2 signaling pathway. Conclusions Based on our findings, RGS 6 aggravates cardiac hypertrophy, and the RGS 6-apoptosis signal-regulating kinase 1 pathway represents a potential therapeutic target to attenuate pressure overload-driven cardiac remodeling.
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