ArticleProceedings of the National Academy of Sciences of the United States of America2010
Cardiac hypertrophy is not amplified by deletion of cGMP-dependent protein kinase I in cardiomyocytes.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
52 citing papers in PubMed, 102 citations in OpenAlex.
- Use of soluble guanylyl cyclase stimulators in heart failure therapy-a mode of action perspective.ESC heart failure · 2026Review
- Soluble guanylate cyclase modulation in heart failure and chronic kidney disease: mechanisms, clinical evidence, and translational boundaries.Frontiers in pharmacology · 2026Review
- The rewiring of cAMP/cGMP and LDH signalling drives cardiac hypertrophy inLife science alliance · 2025Article
- Influence of Soluble Guanylate Cyclase on Cardiac, Vascular, and Renal Structure and Function: A Physiopathological Insight.International journal of molecular sciences · 2025Review
- Angiotensin II-induced cardiac fibrosis and dysfunction are exacerbated by deletion of cGKI in periostin+ myofibroblasts.Clinical science (London, England : 1979) · 2025Article
- Phosphodiesterase in heart and vessels: from physiology to diseases.Physiological reviews · 2024Review
- Article
- Constitutive protein kinase G activation exacerbates stress-induced cardiomyopathy.British journal of pharmacology · 2022Article
- Cyclic GMP and PKG Signaling in Heart Failure.Frontiers in pharmacology · 2022Review
- Guanylyl cyclase-A phosphorylation decreases cardiac hypertrophy and improves systolic function in male, but not female, mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- Cyclic GMP-Dependent Regulation of Vascular Tone and Blood Pressure Involves Cysteine-Rich LIM-Only Protein 4 (CRP4).International journal of molecular sciences · 2021Article
- An update of cyclic nucleotide phosphodiesterase as a target for cardiac diseases.Expert opinion on drug discovery · 2021Review
- Cardiac Cyclic Nucleotide Phosphodiesterases: Roles and Therapeutic Potential in Heart Failure.Cardiovascular drugs and therapy · 2020Review
- cGMP Signaling and Modulation in Heart Failure.Journal of cardiovascular pharmacology · 2020Review
- Mind the gap (junction): cGMP induced by nitric oxide in cardiac myocytes originates from cardiac fibroblasts.British journal of pharmacology · 2019Article
- Phosphodiesterase 2 inhibition preferentially promotes NO/guanylyl cyclase/cGMP signaling to reverse the development of heart failure.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- cGMP Signaling in the Cardiovascular System-The Role of Compartmentation and Its Live Cell Imaging.International journal of molecular sciences · 2018Review
- Newly Identified NO-Sensor Guanylyl Cyclase/Connexin 43 Association Is Involved in Cardiac Electrical Function.Journal of the American Heart Association · 2017Article
- Phosphodiesterase Inhibitors as a Therapeutic Approach to Neuroprotection and Repair.International journal of molecular sciences · 2017Review
- Cardiac Phosphodiesterases and Their Modulation for Treating Heart Disease.Handbook of experimental pharmacology · 2017Review
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6 authors at 5 institutions in 2 countries.
Funding
Abstract
It has been suggested that cGMP kinase I (cGKI) dampens cardiac hypertrophy. We have compared the effect of isoproterenol (ISO) and transverse aortic constriction (TAC) on hypertrophy in WT [control (CTR)] mice, total cGKI-KO mice, and cGKIbeta rescue mice (betaRM) lacking cGKI specifically in cardiomyocytes (CMs). Infusion of ISO did not change the expression of cGKI in the hearts of CTR mice or betaRM but raised the heart weight by approximately 20% in both. An identical hypertrophic growth response was measured in CMs from CTR mice and betaRM and in isolated adult CMs cultured with or without 1 muM ISO. In both genotypes, ISO infusion induced similar changes in the expression of hypertrophy-associated cardiac genes and significant elevation of serum atrial natriuretic peptide and total cardiac cGMP. No differences in cardiac hypertrophy were obtained by 7-day ISO infusion in 4- to 6-week-old conventional cGKI-KO and CTR mice. Furthermore, TAC-induced hypertrophy of CTR mice and betaRM was not different and did not result in changes of the cGMP-hydrolyzing phosphodiesterase activities in hypertropic hearts or CMs. These results strongly suggest that cardiac myocyte cGKI does not affect the development of heart hypertrophy induced by pressure overload or chronic ISO infusion.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.