ArticleThe Journal of clinical investigation2000
CaM kinase signaling induces cardiac hypertrophy and activates the MEF2 transcription factor in vivo.
Article in The Journal of clinical investigation, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 189 papers.
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Who cites it
189 citing papers in PubMed, 520 citations in OpenAlex.
- Review
- Cardiomyocyte YAP represses myocardial inflammation and fibrosis and restrains MEF2-regulated gene expression.American journal of physiology. Heart and circulatory physiology · 2025Article
- Mechanisms of stretch-induced electro-anatomical remodeling and atrial arrhythmogenesis.Journal of molecular and cellular cardiology · 2024Review
- A New linc(-RNA) Between NFAT/MEF2 and Cardiac Hypertrophy.Circulation research · 2024Article
- miR-1 as a Key Epigenetic Regulator in Early Differentiation of Cardiac Sinoatrial Region.International journal of molecular sciences · 2024Article
- Incomplete-penetrant hypertrophic cardiomyopathyProceedings of the National Academy of Sciences of the United States of America · 2024Article
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- Beta Blockade Prevents Cardiac Morphological and Molecular Remodelling in Experimental Uremia.International journal of molecular sciences · 2023Article
- Local decorin delivery via hyaluronic acid microrods improves cardiac performance, ventricular remodeling after myocardial infarction.NPJ Regenerative medicine · 2023Article
- Systematic discovery of transcription factors that improve hPSC-derived cardiomyocyte maturation via temporal analysis of bioengineered cardiac tissues.APL bioengineering · 2023Article
- Immune Cells in Cardiac Injury Repair and Remodeling.Current cardiology reports · 2023Review
- Dynamic chromatin landscape encodes programs for perinatal transition of cardiomyocytes.Cell death discovery · 2023Article
- Cardiac function, structural, and electrical remodeling by microgravity exposure.American journal of physiology. Heart and circulatory physiology · 2023Review
- Ca2+/calmodulin-dependent protein kinase II and protein kinase G oxidation contributes to impaired sarcomeric proteins in hypertrophy model.ESC heart failure · 2022Article
- Programmed Exercise Attenuates Familial Hypertrophic Cardiomyopathy in Transgenic E22K MiceFrontiers in cardiovascular medicine · 2022Article
- Stachydrine hydrochloride ameliorates cardiac hypertrophy through CaMKII/HDAC4/MEF2C signal pathway.American journal of translational research · 2022Article
- Angiotensin II Mediates Cardiomyocyte Hypertrophy in Atrial Cardiomyopathy via Epigenetic Transcriptional Regulation.Computational and mathematical methods in medicine · 2022Article
- Loss of mFrontiers in cardiovascular medicine · 2022Article
- Targeting the forkhead box protein P1 pathway as a novel therapeutic approach for cardiovascular diseases.Heart failure reviews · 2022Review
129 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hypertrophic growth is an adaptive response of the heart to diverse pathological stimuli and is characterized by cardiomyocyte enlargement, sarcomere assembly, and activation of a fetal program of cardiac gene expression. A variety of Ca(2+)-dependent signal transduction pathways have been implicated in cardiac hypertrophy, but whether these pathways are independent or interdependent and whether there is specificity among them are unclear. Previously, we showed that activation of the Ca(2+)/calmodulin-dependent protein phosphatase calcineurin or its target transcription factor NFAT3 was sufficient to evoke myocardial hypertrophy in vivo. Here, we show that activated Ca(2+)/calmodulin-dependent protein kinases-I and -IV (CaMKI and CaMKIV) also induce hypertrophic responses in cardiomyocytes in vitro and that CaMKIV overexpressing mice develop cardiac hypertrophy with increased left ventricular end-diastolic diameter and decreased fractional shortening. Crossing this transgenic line with mice expressing a constitutively activated form of NFAT3 revealed synergy between these signaling pathways. We further show that CaMKIV activates the transcription factor MEF2 through a posttranslational mechanism in the hypertrophic heart in vivo. Activated calcineurin is a less efficient activator of MEF2-dependent transcription, suggesting that the calcineurin/NFAT and CaMK/MEF2 pathways act in parallel. These findings identify MEF2 as a downstream target for CaMK signaling in the hypertrophic heart and suggest that the CaMK and calcineurin pathways preferentially target different transcription factors to induce cardiac hypertrophy.
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Registered trials
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.