ArticleMolecular and cellular biochemistry2003
The myocardial protein S100A1 plays a role in the maintenance of normal gene expression in the adult heart.
Article in Molecular and cellular biochemistry, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
What it found
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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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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.
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.
- Pathophysiological mechanism and therapeutic role of S100 proteins in cardiac failure: a systematic review.Heart failure reviews · 2016Pooled it
- Elevated plasma S100A1 level is a risk factor for ST-segment elevation myocardial infarction and associated with post-infarction cardiac function.International journal of medical sciences · 2019Article
- Cardiac Overexpression of S100A6 Attenuates Cardiomyocyte Apoptosis and Reduces Infarct Size After Myocardial Ischemia-Reperfusion.Journal of the American Heart Association · 2017Article
- S100A1 in human heart failure: lack of recovery following left ventricular assist device support.Circulation. Heart failure · 2014Article
- Therapeutic safety of high myocardial expression levels of the molecular inotrope S100A1 in a preclinical heart failure model.Gene therapy · 2014Article
- Cardiac AAV9-S100A1 gene therapy rescues post-ischemic heart failure in a preclinical large animal model.Science translational medicine · 2011Article
- Modulation of sarcoplasmic reticulum Ca2+ release in skeletal muscle expressing ryanodine receptor impaired in regulation by calmodulin and S100A1.American journal of physiology. Cell physiology · 2011Article
- Intracellular and Extracellular Effects of S100B in the Cardiovascular Response to Disease.Cardiovascular psychiatry and neurology · 2010Article
- Cardiac adenoviral S100A1 gene delivery rescues failing myocardium.The Journal of clinical investigation · 2004Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
S100A1 and S100B are members of a family of 20 kDa Ca2+-binding homodimers that play a role in signal transduction in mammalian cells. S100A1 is the major isoform in normal heart and S100B, normally a brain protein, is induced in hypertrophic myocardium and functions as an intrinsic negative modulator of the hypertrophic response. In order to examine the function of S100A1, we first showed that, in contrast to S100B, S100A1 was downregulated in rat experimental models of myocardial hypertrophy following myocardial infarction or pressure overload. Second, in co-transfection experiments in cultured neonatal rat cardiac myocytes, S100A1 inhibited the alpha1-adrenergic activation of promoters of genes induced during the hypertrophic response including the fetal genes skeletal alpha actin (skACT), and beta-myosin heavy chain (MHC) and S100B, but not the triiodothyronine (T3) activation of the promoter of the alpha-MHC gene, that is normally expressed in adult myocardium. These results suggest that S100A1 is involved in the maintenance of the genetic program that defines normal myocardial function and that its downregulation is permissive for the induction of genes that underlie myocardial hypertrophy.
Indexed as
Identifiers
12619862W1554506243What 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.