ArticleCirculation research2012
Interplay between heart and skeletal muscle disease in heart failure: the 2011 George E. Brown Memorial Lecture.
Article in Circulation research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- Higher skeletal muscle mass is associated with higher blood pressure and left ventricular mass.Journal of hypertension · 2026Article
- Identification of a rare variant in TNNT3 responsible for familial dilated cardiomyopathy through whole-exome sequencing and in silico analysis.European journal of medical research · 2025Article
- Undetected Neuromuscular Disease in Patients after Heart Transplantation.International journal of molecular sciences · 2024Article
- Predictors of infraspinatus muscle degeneration in individuals with an isolated supraspinatus tendon tear.Skeletal radiology · 2023Article
- Smad3 promotes adverse cardiovascular remodeling and dysfunction in doxorubicin-treated hearts.American journal of physiology. Heart and circulatory physiology · 2022Article
- Heme-Induced Oxidation of Cysteine Groups of Myofilament Proteins Leads to Contractile Dysfunction of Permeabilized Human Skeletal Muscle Fibres.International journal of molecular sciences · 2020Article
- The TGF-β pathway mediates doxorubicin effects on cardiac endothelial cells.Journal of molecular and cellular cardiology · 2016Article
- Folliculin (Flcn) inactivation leads to murine cardiac hypertrophy through mTORC1 deregulation.Human molecular genetics · 2014Article
- Exclusive skeletal muscle correction does not modulate dystrophic heart disease in the aged mdx model of Duchenne cardiomyopathy.Human molecular genetics · 2013Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The study of single gene disorders often provides insight for more complex human disease. Mutations in the genes encoding the dystrophin protein complex cause muscular dystrophy and cardiomyopathy by destabilizing the plasma membrane of skeletal myofibers and cardiomyocytes. In these diseases, progressive skeletal muscle degeneration and weakness contribute to cardiac dysfunction. Moreover, the pace and pattern of muscle weakness, along with onset of cardiomyopathy, is highly variable even when associated with the same identical mutation. Using a mouse model of muscular dystrophy and cardiomyopathy, we identified genetic loci that modify muscle pathology and cardiac fibrosis. Distinct genetic modifiers were identified for diaphragm and abdominal musculature, and these genetic intervals differ from those that regulate pathology in the skeletal muscle of the limbs and the heart. One modifier gene was identified and highlights the importance of the transforming growth factor-β pathway in the pathogenesis of muscular dystrophy and cardiomyopathy. We determined that canonical transforming growth factor-β signaling contributes to heart and muscle dysfunction using a Drosophila model. Together, these studies demonstrate the value of using a genetically sensitized model to uncover pathways that regulate heart failure and muscle weakness.
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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.