ArticleThe American journal of pathology2002
Extensive induction of important mediators of fibrosis and dystrophic calcification in desmin-deficient cardiomyopathy.
Article in The American journal of pathology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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
19 citing papers in PubMed, 53 citations in OpenAlex.
- Heart of Stone: Rare Case of Incidentally Detected Endocardial Calcification.Methodist DeBakey cardiovascular journal · 2025Article
- Common and Key Differential Pathogenic Pathways in Desminopathy and Titinopathy.International journal of medical sciences · 2024Article
- Desmin Reorganization by Stimuli Inducing Oxidative Stress and Electrophiles: Role of Its Single Cysteine Residue.Antioxidants (Basel, Switzerland) · 2023Article
- Targeting the cytoskeleton and extracellular matrix in cardiovascular disease drug discovery.Expert opinion on drug discovery · 2022Review
- Myospryn deficiency leads to impaired cardiac structure and function and schizophrenia-associated symptoms.Cell and tissue research · 2021Article
- Intermediate filaments in cardiomyopathy.Biophysical reviews · 2018Review
- Type III Intermediate Filaments Desmin, Glial Fibrillary Acidic Protein (GFAP), Vimentin, and Peripherin.Cold Spring Harbor perspectives in biology · 2017Review
- Desmin and αB-crystallin interplay in the maintenance of mitochondrial homeostasis and cardiomyocyte survival.Journal of cell science · 2016Article
- Fabrication of cell-laden macroporous biodegradable hydrogels with tunable porosities and pore sizes.Tissue engineering. Part C, Methods · 2015Article
- Osteopontin: At the cross-roads of myocyte survival and myocardial function.Life sciences · 2014Review
- Μyospryn: a multifunctional desmin-associated protein.Histochemistry and cell biology · 2013Review
- Matricellular proteins in cardiac adaptation and disease.Physiological reviews · 2012Review
- Azelnidipine protects myocardium in hyperglycemia-induced cardiac damage.Cardiovascular diabetology · 2010Article
- Myocardial oxidative stress, osteogenic phenotype, and energy metabolism are differentially involved in the initiation and early progression of delta-sarcoglycan-null cardiomyopathy.Molecular and cellular biochemistry · 2009Article
- A missense mutation in desmin tail domain linked to human dilated cardiomyopathy promotes cleavage of the head domain and abolishes its Z-disc localization.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2008Article
- Cardiac dysfunction in aging conscious rats: altered cardiac cytoskeletal proteins as a potential mechanism.American journal of physiology. Heart and circulatory physiology · 2008Article
- Calcification of myocardial necrosis is common in mice.Virchows Archiv : an international journal of pathology · 2006Article
- Desmin filaments influence myofilament spacing and lateral compliance of slow skeletal muscle fibers.Biophysical journal · 2005Article
- A locus on chromosome 7 determines dramatic up-regulation of osteopontin in dystrophic cardiac calcification in mice.The American journal of pathology · 2004Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Mice lacking the intermediate filament protein desmin demonstrate abnormal mitochondria behavior, disruption of muscle architecture, and myocardial degeneration with extensive calcium deposits and fibrosis. These abnormalities are associated with cardiomyocyte hypertrophy, cardiac chamber dilation and eventually with heart failure. In an effort to elucidate the molecular mechanisms leading to the observed pathogenesis, we have analyzed gene expression changes in cardiac tissue using differential display polymerase chain reaction and cDNA atlas array methods. The most substantial changes were found in genes coding the small extracellular matrix proteins osteopontin and decorin that are dramatically induced in the desmin-null myocardium. We further analyzed their expression pattern both at the RNA and protein levels and we compared their spatial expression with the onset of calcification. Extensive osteopontin localization is observed by immunohistochemistry in the desmin-null myocardium in areas with massive myocyte death, as well as in hypercellular regions with variable degrees of calcification and fibrosis. Osteopontin is consistently co-localized with calcified deposits, which progressively are transformed to psammoma bodies surrounded by decorin, especially in the right ventricle. These data together with the observed up-regulation of transforming growth factor-beta1 and angiotensin-converting enzyme, could explain the extensive fibrosis and dystrophic calcification observed in the heart of desmin-null mice, potentially crucial events leading to heart failure.
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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.