Serological evidence of altered collagen homeostasis reflects early ventricular remodeling following acute myocardial infarction

McGavigan, Andrew D.; Maxwell, Paul R.; Dunn, Francis G.

doi:10.1016/j.ijcard.2005.08.045

Cited by 14 publications

(10 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Recently, Zhou et al [9] have reported that phenytoin can attenuate the adverse ventricular remodeling after myocardial infarction in rat, possibly by facilitating and strengthen extracellular matrix deposition. The findings of McGavigan et al [3] may be considered to be compatible with these previously reported data.…”

supporting

confidence: 88%

“…Recently, McGavigan et al [3] have evaluated the role of impaired collagen homeostasis in predicting the development of early ventricular remodeling following acute myocardial infarction. Fifty-one patients with acute myocardial infarction have been included in this study.…”

mentioning

confidence: 99%

“…Although the subject of McGavigan et al's [3] article is original and the obtained data are exciting, there a some methodologic weaknesses, limiting the reliability of the findings. The most important one is the heterogeneous study groups regarding the localization of myocardial infarction.…”

mentioning

confidence: 99%

See 2 more Smart Citations

Ventricular remodeling following acute myocardial infarction: The role of altered collagen homeostasis

Turhan

Aksoy

Yetkın

et al. 2007

International Journal of Cardiology

View full text Add to dashboard Cite

supporting

confidence: 88%

mentioning

confidence: 99%

See 1 more Smart Citation

Ventricular remodeling following acute myocardial infarction: The role of altered collagen homeostasis

Turhan

Aksoy

Yetkın

et al. 2007

International Journal of Cardiology

View full text Add to dashboard Cite

“…13–17 Multiple studies have suggested matricryptins could be potential therapeutic targets for heart failure patients. 14, 18, 19 Below, we summarize our currently knowledge on the involvement of MMPs in post-MI remodeling.…”

Section: Mmps As Biomarkers For Heart Failurementioning

confidence: 99%

Matrix Metalloproteinases in Myocardial Infarction and Heart Failure

DeLeon‐Pennell

Meschiari

Jung

et al. 2017

Progress in Molecular Biology and Translational Science

218

188

View full text Add to dashboard Cite

Cardiovascular disease (CVD) is the leading cause of death, accounting for 600,000 deaths each year in the U.S. In addition, heart failure accounts for 37% of healthcare spending. Matrix metalloproteinases (MMPs) increase after myocardial infarction (MI) and correlate with left ventricular dysfunction in heart failure patients. MMPs regulate the remodeling process by facilitating extracellular matrix (ECM) turnover and inflammatory signaling. Due to the critical role MMPs play during cardiac remodeling, there is a need to better understand the pathophysiological mechanism of MMPs, including the biological function of the downstream products of MMP proteolysis. Future studies developing new therapeutic targets that inhibit specific MMP actions to limit the development of heart failure post-MI are warranted. This book chapter focuses on the role of MMPs post-MI, the efficiency of MMPs as biomarkers for MI or heart failure, and the future of MMPs and their cleavage products as targets for prevention of post-MI heart failure.

show abstract

“…McGavigan and colleagues measured PICP and CITP, markers of collagen I synthesis and degradation, respectively, in 51 patients with acute MI. [29] When dichotomized to wall motion index, patients with abnormal wall motion index showed higher baseline levels of CITP and decreased levels of PICP, indicating a net increase in collagen I breakdown. Francisco Villarreal and colleagues assessed the time course of collagen I degradation post-MI in pigs.…”

Section: Soluble Ecm Fragments Are Generated Post-mimentioning

confidence: 99%

Extracellular matrix turnover and signaling during cardiac remodeling following MI: Causes and consequences

Zamilpa

Lindsey

2010

Journal of Molecular and Cellular Cardiology

View full text Add to dashboard Cite

The concept that extracellular matrix (ECM) turnover occurs during cardiac remodeling is a wellaccepted paradigm. To date, a multitude of studies document that remodeling is accompanied by increases in the synthesis and deposition of ECM components as well as increases in extracellular proteases, especially matrix metalloproteinases (MMPs), which break down ECM components. Further, soluble ECM fragments generated from enzymatic action serve to stimulate cell behavior and have been proposed as candidate plasma biomarkers of cardiac remodeling. This review briefly summarizes our current knowledge base on cardiac ECM turnover following myocardial infarction (MI), but more importantly extends discussion by defining avenues that remain to be explored to drive the ECM remodeling field forward. Specifically, this review will discuss cause and effect roles for the ECM changes observed following MI and the potential role of the ECM changes that may serve as trigger points to regulate remodeling. While the pattern of remodeling following MI is qualititatively similar but quantitively different from various types of injury, the basic theme in remodeling is repeated. Therefore, while we use the MI model as the prototype injury model, the themes discussed here are also relevant to cardiac remodeling due to other types of injury.

show abstract

Serological evidence of altered collagen homeostasis reflects early ventricular remodeling following acute myocardial infarction

Cited by 14 publications

References 43 publications

Ventricular remodeling following acute myocardial infarction: The role of altered collagen homeostasis

Ventricular remodeling following acute myocardial infarction: The role of altered collagen homeostasis

Matrix Metalloproteinases in Myocardial Infarction and Heart Failure

Extracellular matrix turnover and signaling during cardiac remodeling following MI: Causes and consequences

Contact Info

Product

Resources

About