ReviewHeart failure reviews2004
Myocardial remodeling in viral heart disease: possible interactions between inflammatory mediators and MMP-TIMP system.
Review in Heart failure reviews, 2004. 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, 54 citations in OpenAlex.
- Luteolin Protects Cardiomyocytes Cells against Lipopolysaccharide-Induced Apoptosis and Inflammatory Damage by Modulating Nlrp3.Yonsei medical journal · 2022Article
- Farrerol prevents Angiotensin II-induced cardiac remodelingFrontiers in pharmacology · 2022Article
- Mechanisms and Therapeutic Strategies of Viral Myocarditis Targeting Autophagy.Frontiers in pharmacology · 2022Review
- Article
- Effect of prostaglandin analogs: Latanoprost, bimatoprost, and unoprostone on matrix metalloproteinases and their inhibitors in human trabecular meshwork endothelial cells.Experimental eye research · 2020Article
- What Is the Arrhythmic Substrate in Viral Myocarditis? Insights from Clinical and Animal Studies.Frontiers in physiology · 2016Review
- Targeting matrix metalloproteinase activity and expression for the treatment of viral myocarditis.Journal of cardiovascular translational research · 2014Review
- The role of the proteasome in heart disease.Biochimica et biophysica acta · 2011Review
- Animal models of cardiac disease and stem cell therapy.The open cardiovascular medicine journal · 2010Article
- Molecular determinants of the cardiometabolic phenotype.Endocrine, metabolic & immune disorders drug targets · 2010Review
- Antimicrobial agents for myocarditis: target the pathway, not the pathogen.Heart (British Cardiac Society) · 2010Article
- Review
- Acute viral myocarditis.European heart journal · 2008Review
- Amelioration of coxsackievirus B3-mediated myocarditis by inhibition of tissue inhibitors of matrix metalloproteinase-1.The American journal of pathology · 2007Article
- Inflammation, ECG changes and pericardial effusion: whom to biopsy in suspected myocarditis?Clinical research in cardiology : official journal of the German Cardiac Society · 2006Review
- Increased cardiac mRNA expression of matrix metalloproteinase-1 (MMP-1) and its inhibitor (TIMP-1) in DCM patients.Clinical research in cardiology : official journal of the German Cardiac Society · 2006Article
- Loss or inhibition of uPA or MMP-9 attenuates LV remodeling and dysfunction after acute pressure overload in mice.The American journal of pathology · 2005Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Matrix metalloproteinases (MMP), a family of proteases, are involved in the degradation of extracellular matrix proteins and hence in the determination of interstitial architecture. In the heart, MMPs have been found to play a significant role in the development of myocardial remodeling and congestive heart failure. Tissue inhibitors of matrix metalloproteinases (TIMPs) represent a family of proteins which are known to regulate the expression and activity of MMPs. TIMPs are endogenous physiological inhibitors of MMPs and their concomitant downregulation in heart failure suggests the existence of a critical balance between MMPs and TIMPs in the normal maintenance of myocardial interstitial homeostasis. In addition, cytokines regulate expression of both MMPs and TIMPs besides eliciting a direct effect on myocardial cell function. Therefore, myocardial inflammation may also contribute to the development of cardiac remodeling along with other stimuli like mechanical stress and humoral factors. Viral myocarditis, a predisposing factor for dilated cardiomyopathy, is a condition in which extent of intramyocardial inflammation is thought to determine the progression of disease. Inflammatory events in the heart following viral infection are speculated to be responsible for the transition of myocarditis to dilated cardiomyopathy. In viral myocarditis and other inflammatory heart diseases, the inflammatory cells and their battery of cytokines may also alter the myocardial MMP-TIMP system and eventually lead to dilation of the heart and ventricular dysfunction. The objective of this review is to present an overall picture of the inflammatory phase in viral myocarditis and discuss the possible interactions between inflammation and myocardial MMP profiles which may lead to the evolution of dilated cardiomyopathy.
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.