ArticleProceedings of the National Academy of Sciences of the United States of America2009
Myocardin is required for cardiomyocyte survival and maintenance of heart function.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
67 citing papers in PubMed, 1 synthesis or guideline pooled it, 102 citations in OpenAlex.
- Gene expression profiling of HGF/Met activation in neonatal mouse heart.Transgenic research · 2013Pooled it
- Spatial expression of myocardin protein in normal and disease states.American journal of physiology. Cell physiology · 2026Article
- Review
- Article
- Defective mesenchymal Bmpr1a-mediated BMP signaling causes congenital pulmonary cysts.bioRxiv : the preprint server for biology · 2024Article
- Coactivator condensation drives cardiovascular cell lineage specification.Science advances · 2024Article
- Role of ZIP kinase in development of myofibroblast differentiation from HPMCs.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Myocardial infarction in rats was alleviated by MSCs derived from the maternal segment of the human umbilical cord.Frontiers in cell and developmental biology · 2024Article
- Article
- Actin-related protein 5 suppresses the cooperative activation of cardiac gene transcription by myocardin and MEF2.FEBS open bio · 2023Article
- Dilated cardiomyopathy: a new insight into the rare but common cause of heart failure.Heart failure reviews · 2022Review
- Non-Coding RNAs: Prevention, Diagnosis, and Treatment in Myocardial Ischemia-Reperfusion Injury.International journal of molecular sciences · 2022Review
- Telomerase/myocardin expressing mesenchymal cells induce survival and cardiovascular markers in cardiac stromal cells undergoing ischaemia/reperfusion.Journal of cellular and molecular medicine · 2021Article
- NG2/CSPG4, CD146/MCAM and VAP1/AOC3 are regulated by myocardin-related transcription factors in smooth muscle cells.Scientific reports · 2021Article
- LncRNAs in Cardiomyocyte Maturation: New Window for Cardiac Regenerative Medicine.Non-coding RNA · 2021Review
- Exosomal LINC00174 derived from vascular endothelial cells attenuates myocardial I/R injury via p53-mediated autophagy and apoptosis.Molecular therapy. Nucleic acids · 2021Article
- Sall4 and Myocd Empower Direct Cardiac Reprogramming From Adult Cardiac Fibroblasts After Injury.Frontiers in cell and developmental biology · 2021Article
- SUMO proteins in the cardiovascular system: friend or foe?Journal of biomedical science · 2020Review
- Cardiomyocyte Maturation: New Phase in Development.Circulation research · 2020Review
- Loss-of-function variants in myocardin cause congenital megabladder in humans and mice.The Journal of clinical investigation · 2019Article
7 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Despite intense investigation over the past century, the molecular mechanisms that regulate maintenance and adaptation of the heart during postnatal development are poorly understood. Myocardin is a remarkably potent transcriptional coactivator expressed exclusively in cardiac myocytes and smooth muscle cells during postnatal development. Here we show that myocardin is required for maintenance of cardiomyocyte structure and sarcomeric organization and that cell-autonomous loss of myocardin in cardiac myocytes triggers programmed cell death. Mice harboring a cardiomyocyte-restricted null mutation in the myocardin gene (Myocd) develop dilated cardiomyopathy and succumb from heart failure within a year. Remarkably, ablation of the Myocd gene in the adult heart leads to the rapid-onset of heart failure, dilated cardiomyopathy, and death within a week. Myocd gene ablation is accompanied by dissolution of sarcomeric organization, disruption of the intercalated disc, and cell-autonomous loss of cardiomyocytes via apoptosis. Expression of myocardin/serum response factor-regulated myofibrillar genes is extinguished, or profoundly attenuated, in myocardin-deficient hearts. Conversely, proapoptotic factors are induced and activated in myocardin-deficient hearts. We conclude that the transcriptional coactivator myocardin is required for maintenance of heart function and ultimately cardiomyocyte survival.
Indexed as
Identifiers
What OpenQuestion holds
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.