ArticleAmerican journal of physiology. Heart and circulatory physiology2010
Calmodulin kinase II is required for angiotensin II-mediated vascular smooth muscle hypertrophy.
Article in American journal of physiology. Heart and circulatory physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 78 citations in OpenAlex.
- Article
- Role of the Renin-Angiotensin System in Blood Pressure Regulation in Smooth Muscle-Specific Cullin-3 Deficient Mice.Hypertension (Dallas, Tex. : 1979) · 2025Article
- CaInflammation and regeneration · 2025Review
- The advances in acetylation modification in senescence and aging-related diseases.Frontiers in physiology · 2025Review
- Epigenetic DNA Methylation and Protein Homocysteinylation: Key Players in Hypertensive Renovascular Damage.International journal of molecular sciences · 2024Review
- Role of CaMKII in diabetes induced vascular injury and its interaction with anti-diabetes therapy.Reviews in endocrine & metabolic disorders · 2024Review
- Molecular Mechanisms in Genetic Aortopathy-Signaling Pathways and Potential Interventions.International journal of molecular sciences · 2023Review
- CaMKII Splice Variants in Vascular Smooth Muscle Cells: The Next Step or Redundancy?International journal of molecular sciences · 2022Review
- HDAC4 Inhibitors as Antivascular Senescence Therapeutics.Oxidative medicine and cellular longevity · 2022Review
- Article
- Cardiac Gq Receptors and Calcineurin Activation Are Not Required for the Hypertrophic Response to Mechanical Left Ventricular Pressure Overload.Frontiers in cell and developmental biology · 2021Article
- Chronic Intermittent Hypoxia Regulates CaMKII-Dependent MAPK Signaling to Promote the Initiation of Abdominal Aortic Aneurysm.Oxidative medicine and cellular longevity · 2021Article
- An Insight on Multicentric Signaling of Angiotensin II in Cardiovascular system: A Recent Update.Frontiers in pharmacology · 2021Review
- A GSK3-SRF Axis Mediates Angiotensin II Induced Endothelin Transcription in Vascular Endothelial Cells.Frontiers in cell and developmental biology · 2021Article
- Lysine acetyltransferases and lysine deacetylases as targets for cardiovascular disease.Nature reviews. Cardiology · 2020Review
- Camk2n1 Is a Negative Regulator of Blood Pressure, Left Ventricular Mass, Insulin Sensitivity, and Promotes Adiposity.Hypertension (Dallas, Tex. : 1979) · 2019Article
- Histone deacetylase inhibitor LMK235 attenuates vascular constriction and aortic remodelling in hypertension.Journal of cellular and molecular medicine · 2019Article
- Selective inhibition of histone deacetylase 8 improves vascular hypertrophy, relaxation, and inflammation in angiotensin II hypertensive mice.Clinical hypertension · 2019Article
- Angiotensin II Signal Transduction: An Update on Mechanisms of Physiology and Pathophysiology.Physiological reviews · 2018Review
- Gallic acid attenuates calcium calmodulin-dependent kinase II-induced apoptosis in spontaneously hypertensive rats.Journal of cellular and molecular medicine · 2018Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Despite our understanding that medial smooth muscle hypertrophy is a central feature of vascular remodeling, the molecular pathways underlying this pathology are still not well understood. Work over the past decade has illustrated a potential role for the multifunctional calmodulin-dependent kinase CaMKII in smooth muscle cell contraction, growth, and migration. Here we demonstrate that CaMKII is enriched in vascular smooth muscle (VSM) and that CaMKII inhibition blocks ANG II-dependent VSM cell hypertrophy in vitro and in vivo. Specifically, systemic CaMKII inhibition with KN-93 prevented ANG II-mediated hypertension and medial hypertrophy in vivo. Adenoviral transduction with the CaMKII peptide inhibitor CaMKIIN abrogated ANG II-induced VSM hypertrophy in vitro, which was augmented by overexpression of CaMKII-delta2. Finally, we identify the downstream signaling components critical for ANG II- and CaMKII-mediated VSM hypertrophy. Specifically, we demonstrate that CaMKII induces VSM hypertrophy by regulating histone deacetylase 4 (HDAC4) activity, thereby stimulating activity of the hypertrophic transcription factor MEF2. MEF2 transcription is activated by ANG II in vivo and abrogated by the CaMKII inhibitor KN-93. Together, our studies identify a complete pathway for ANG II-triggered arterial VSM hypertrophy and identify new potential therapeutic targets for chronic human hypertension.
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