ArticleInternational journal of experimental pathology2010
Myostatin and follistatin expression in skeletal muscles of rats with chronic heart failure.
Article in International journal of experimental pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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
18 citing papers in PubMed, 46 citations in OpenAlex.
- Myostatin and the Heart.Biomolecules · 2023Review
- Gut microbiota in sarcopenia and heart failure.The journal of cardiovascular aging · 2022Article
- Pharmacological management of cardiac cachexia: a review of potential therapy options.Heart failure reviews · 2019Review
- Effects of growth hormone on cardiac remodeling and soleus muscle in rats with aortic stenosis-induced heart failure.Oncotarget · 2017Article
- Review
- Cardiac Cachexia: Perspectives for Prevention and Treatment.Arquivos brasileiros de cardiologia · 2017Review
- Ramipril attenuates left ventricular remodeling by regulating the expression of activin A-follistatin in a rat model of heart failure.Scientific reports · 2016Article
- FSTL1 as a Potential Mediator of Exercise-Induced Cardioprotection in Post-Myocardial Infarction Rats.Scientific reports · 2016Article
- Activins and Inhibins: Roles in Development, Physiology, and Disease.Cold Spring Harbor perspectives in biology · 2016Review
- Association between Functional Variables and Heart Failure after Myocardial Infarction in Rats.Arquivos brasileiros de cardiologia · 2016Article
- Beneficial Effects of Physical Exercise on Functional Capacity and Skeletal Muscle Oxidative Stress in Rats with Aortic Stenosis-Induced Heart Failure.Oxidative medicine and cellular longevity · 2016Article
- Rutin administration attenuates myocardial dysfunction in diabetic rats.Cardiovascular diabetology · 2015Article
- Cardiac myostatin upregulation occurs immediately after myocardial ischemia and is involved in skeletal muscle activation of atrophy.Biochemical and biophysical research communications · 2015Article
- Low Intensity Physical Exercise Attenuates Cardiac Remodeling and Myocardial Oxidative Stress and Dysfunction in Diabetic Rats.Journal of diabetes research · 2015Article
- Inhibin at 90: from discovery to clinical application, a historical review.Endocrine reviews · 2014Review
- Diabetes mellitus activates fetal gene program and intensifies cardiac remodeling and oxidative stress in aged spontaneously hypertensive rats.Cardiovascular diabetology · 2013Article
- Myostatin from the heart: local and systemic actions in cardiac failure and muscle wasting.American journal of physiology. Heart and circulatory physiology · 2011Review
- Exercise training improves the IL-10/TNF-α cytokine balance in the gastrocnemius of rats with heart failure.Brazilian journal of physical therapyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Skeletal muscle abnormalities can contribute to decreased exercise capacity in heart failure. Although muscle atrophy is a common alteration in heart failure, the mechanisms responsible for muscle mass reduction are not clear. Myostatin, a member of TGF-beta family (transforming growth factor), regulates muscle growth and mass. Several studies have shown a negative correlation between myostatin expression and muscle mass. The aim of this study was to evaluate myostatin expression in skeletal muscles of rats with heart failure. As myostatin gene expression can be modulated by follistatin, we also evaluated its expression. Heart failure was induced by myocardial infarction (MI, n = 10); results were compared to Sham-operated group (n = 10). Ventricular function was assessed by echocardiogram. Gene expression was analyzed by real-time PCR and protein levels by Western blotting in the soleus and gastrocnemius muscles; fibre trophism was evaluated by morphometric analysis. MI group presented heart failure evidence such as pleural effusion and right ventricular hypertrophy. Left ventricular dilation and dysfunction were observed in MI group. In the soleus muscle, cross-sectional area (P = 0.006) and follistatin protein levels (Sham 1.00 +/- 0.36; MI 0.18 +/- 0.06 arbitrary units; P = 0.03) were lower in MI and there was a trend for follistatin gene expression to be lower in MI group (P = 0.085). There was no change in myostatin expression between groups. In gastrocnemius, all MI group parameters were statistically similar to the Sham. In conclusion, our data show that during chronic heart failure, decreased skeletal muscle trophism is combined with unchanged myostatin and reduced follistatin expression.
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.