Matrix metalloproteinase-1 promoter polymorphisms and changes in left ventricular volume following acute myocardial infarction

Martin, Thomas N.; Penney, Dawn E.; Smith, Jamie; Groenning, Bjoern A.; Dargie, Henry J.; Hillis, Graham S.

doi:10.1016/j.amjcard.2004.06.064

Cited by 14 publications

(6 citation statements)

References 13 publications

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“…In patients with DCM, a relationship between the 1360C/T MMP-2 polymorphism and clinical aspects of disease progression could not be identified (277). In a preliminary clinical study, the addition of a guanine within the MMP-1 promoter region (Ϫ1607 1G/2G) was associated within an acceleration of adverse LV myocardial remodeling in patients post-MI (258). In another study, certain single nucleotide polymorphisms within the MMP-1 promoter that may actually reduce MMP-1 transcriptional activity were identified and associated with reduced risk of MI (329).…”

Section: Gene Polymorphism Observationsmentioning

confidence: 99%

“…Clinical studies have now identified variant forms contained within the DNA sequences of MMP genes, or polymorphisms, for several of the MMP subtypes (25,30,65,163,240,241,258,273,277,304,329,377,440,466,514,539). The polymorphisms that have been identified thus far often affect the promoter region of the MMP gene, and thereby influence critical steps in the binding of transcription factors or the overall efficiency of transcription.…”

Section: Gene Polymorphism Observationsmentioning

confidence: 99%

See 1 more Smart Citation

Myocardial Matrix Remodeling and the Matrix Metalloproteinases: Influence on Cardiac Form and Function

Spinale¹

2007

Physiological Reviews

998

1,023

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It is now becoming apparent that dynamic changes occur within the interstitium that directly contribute to adverse myocardial remodeling following myocardial infarction (MI), with hypertensive heart disease and with intrinsic myocardial disease such as cardiomyopathy. Furthermore, a family of matrix proteases, the matrix metalloproteinases (MMPs) and the tissue inhibitors of MMPs (TIMPs), has been recognized to play an important role in matrix remodeling in these cardiac disease states. The purpose of this review is fivefold: 1) to examine and redefine the myocardial matrix as a critical and dynamic entity with respect to the remodeling process encountered with MI, hypertension, or cardiomyopathic disease; 2) present the remarkable progress that has been made with respect to MMP/TIMP biology and how it relates to myocardial matrix remodeling; 3) to evaluate critical translational/clinical studies that have provided a cause-effect relationship between alterations in MMP/TIMP regulation and myocardial matrix remodeling; 4) to provide a critical review and analysis of current diagnostic, prognostic, and pharmacological approaches that utilized our basic understanding of MMP/TIMPs in the context of cardiac disease; and 5) most importantly, to dispel the historical belief that the myocardial matrix is a passive structure and supplant this belief that the regulation of matrix protease pathways such as the MMPs and TIMPs will likely yield a new avenue of diagnostic and therapeutic strategies for myocardial remodeling and the progression to heart failure.

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Section: Gene Polymorphism Observationsmentioning

confidence: 99%

Section: Gene Polymorphism Observationsmentioning

confidence: 99%

Myocardial Matrix Remodeling and the Matrix Metalloproteinases: Influence on Cardiac Form and Function

Spinale¹

2007

Physiological Reviews

998

1,023

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“…Martin et al . reported a statistically significant association between carriers of the 2G polymorphism and increased risk of remodelling after MI [24]. …”

Section: Discussionmentioning

confidence: 99%

“…MMP1 can degrade collagens type I and III and its expression significantly increases in atherosclerotic plaque characterized by having a thin fibrous cap [23]. The MMP1 GG/GG polymorphism is associated with enhanced translation into functional MMP1 [24], so we postulated that this polymorphism can promote atherosclerotic plaque rupture.…”

Section: Introductionmentioning

confidence: 99%

Original research Genetic variability and the risk of myocardial infarction in Poles under 45 years of age

Sakowicz¹,

Fendler²,

Lelonek³

et al. 2010

aoms

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IntroductionMyocardial infarction is caused by the obstruction of an artery in places of atherosclerosis plaque rupture. Endothelial cells during their activation express chemoattractant and adhesion molecules whereas infiltrating inflammatory cells produce enzymes, predisposing a lesion to rupture.Material and methodsWe investigated the correlation between polymorphisms in the human genes E-selectin (Ser128Arg), ICAM1 (K469E), OLR1 (K167N), MMP1 (1G/2G) and MMP3 (−1612 5A/6A) and the risk of MI in young Poles under 45 years. There was no significant difference in the frequency of single nucleotide polymorphism (SNP) of the studied genes E-selectin (Ser128Arg), ICAM1 (K469E), OLR1 (K167N) and MMP3 (−1612 5A/6A) between patients with MI and controls.ResultsThe analysis of the association of the 1G2G polymorphism with the risk of myocardial infarction indicated an odds ratio (OR) of 5.68 (95% confidence interval [95% CI] 2.60 to 12.36). Other factors associated with myocardial infarction were: smoking (OR 4.12; 95% CI 1.63–10.44), male sex (OR 16.02; 95% CI 5.90–43.46), hypercholesterolaemia (OR 2.74; 95% CI 1.29–5.83) and arterial hypertension (OR 4.56; 95% CI 1.66–14.47).ConclusionsWe found that only MMP1 1G/2G polymorphism is associated with myocardial infarction in the Polish population of individuals younger than 45 years. Clinical factors seemed to play a greater role in the analysed group.

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“…В исследовании, где у 42 больных жителей Шотландии, перенесших первый ИМ, изучали связь между ремоделированием левого желудочка и полиморфизмом инсерции/делеции сайта -1607 MMP-1, выявлено, что носители гомозиготного генотипа 2G/2G имели повышенный риск ремоделирования по сравнению с гомозиготами 1G/1G и гетерозиготами 1G/2G [25].…”

Section: матриксные металлопротеазы и тканевой ингибитор металлопроте...unclassified

Some molecular genetic risk factors for myocardial fibrosis (Literature review)

Гриценко

Чумакова

Понасенко

et al. 2022

SJCEM

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Matrix metalloproteinase-1 promoter polymorphisms and changes in left ventricular volume following acute myocardial infarction

Cited by 14 publications

References 13 publications

Myocardial Matrix Remodeling and the Matrix Metalloproteinases: Influence on Cardiac Form and Function

Myocardial Matrix Remodeling and the Matrix Metalloproteinases: Influence on Cardiac Form and Function

Original research Genetic variability and the risk of myocardial infarction in Poles under 45 years of age

Some molecular genetic risk factors for myocardial fibrosis (Literature review)

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