ArticleCardiology2010
Imbalance of matrix metalloproteinases/tissue inhibitor of metalloproteinase-1 and loss of fibronectin expression in patients with congestive heart failure.
Article in Cardiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 24 citations in OpenAlex.
- TFAM overexpression reduces pathological cardiac remodeling.Molecular and cellular biochemistry · 2019Article
- Impact of losartan and angiotensin II on the expression of matrix metalloproteinase-9 and tissue inhibitor of metalloproteinase-1 in rat vascular smooth muscle cells.Molecular medicine reports · 2015Article
- Dysregulation of Mfn2 and Drp-1 proteins in heart failure.Canadian journal of physiology and pharmacology · 2014Review
- Matrix metalloproteinases and their tissue inhibitors in hypertension-related pregnancy complications.Journal of human hypertension · 2013Review
- Role of various proteases in cardiac remodeling and progression of heart failure.Heart failure reviews · 2012Review
- Comparative analysis of oncofetal fibronectin and tenascin-C expression in right atrial auricular and left ventricular human cardiac tissue from patients with coronary artery disease and aortic valve stenosis.Histochemistry and cell biology · 2011Article
- Tipping the extracellular matrix balance during heart failure progression: do we always go right?Cardiology · 2010Article
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivePrevious studies have demonstrated that an imbalance of matrix metalloproteinases (MMPs)/tissue inhibitors of metalloproteinase-1 (TIMP-1) and a loss of fibronectin are associated with postmyocardial infarction remodeling in rats. The present study was designed to examine this issue in patients with congestive heart failure (CHF).
methodsWe measured plasma levels and the cardiac protein expression of MMPs/TIMP-1 and fibronectin in 39 patients with CHF and 38 controls.
resultsPlasma levels of MMP-2, MMP-3, and MMP-9 tended to be higher in patients with CHF (NYHA II: 276 +/- 18, 613 +/- 118, and 245 +/- 43 microg/l, respectively; NYHA III: 302 +/- 20, 850 +/- 132, and 310 +/- 39 microg/l, respectively; NYHA IV: 367 +/- 15, 998 +/- 99, and 392 +/- 27 microg/l, respectively) than in controls (213 +/- 23, 485 +/- 102, and 158 +/- 31 microg/l, respectively), while the plasma TIMP-1 level tended to be lower in patients with CHF (NYHA II: 126 +/- 12 microg/l, NYHA III: 83 +/- 11 microg/l, and NYHA IV: 61 +/- 12 microg/l) than in controls (208 +/- 15 microg/l). Interestingly, the changes in protein expression of MMPs/TIMP-1 were consistent with their plasma concentration. Furthermore, the fibronectin level in the patients with CHF was significantly lower than in the controls.
conclusionsThese data suggest that human CHF is associated with an imbalance of MMPs/TIMP-1 and a concurrent loss of fibronectin.
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