71 Cardiac matrix remodelling in congestive heart failure: the role of matrix metalloproteinase (MMPs)

Abou‐Raya, S.; Naeem, Amr; Marzouk, Salah

doi:10.1016/s1567-4215(03)90014-2

Cited by 6 publications

(6 citation statements)

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“…Furthermore, quantification of certain MMPs and their inhibitors in blood has been correlated with the degree of atherogenesis in humans (120). The MMPs are also involved in several non-atherosclerotic processes within the heart (121)(122)(123)(124)(125)(126). Most importantly, as previously mentioned, disruption of the IEL as a result of the adventitia/media infiltrated by monocytes, which release MMPs mostly at areas of neovascularization.…”

Section: Plaque Rupturementioning

confidence: 99%

Atherothrombosis and High-Risk Plaque

Fuster

Moreno

Fayad

et al. 2005

Journal of the American College of Cardiology

682

433

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Atherothrombosis is a complex disease in which cholesterol deposition, inflammation, and thrombus formation play a major role. Rupture of high-risk, vulnerable plaques is responsible for coronary thrombosis, the main cause of unstable angina, acute myocardial infarction, and sudden cardiac death. In addition to rupture, plaque erosion may also lead to occlusive thrombosis and acute coronary events. Atherothrombosis can be evaluated according to histologic criteria, most commonly categorized by the American Heart Association (AHA) classification. However, this classification does not include the thin cap fibroatheroma, the most common form of high-risk, vulnerable plaque. Furthermore, the AHA classification does not include plaque erosion. As a result, new classifications have emerged and are reviewed in this article. The disease is asymptomatic during a long period and dramatically changes its course when complicated by thrombosis. This is summarized in five phases, from early lesions to plaque rupture, followed by plaque healing and fibrocalcification. For the early phases, the role of endothelial dysfunction, cholesterol transport, high-density lipoprotein, and proteoglycans are discussed. Furthermore, the innate and adaptive immune response to autoantigens, the Toll-like receptors, and the mechanisms of calcification are carefully analyzed. For the advanced phases, the role of eccentric remodeling, vasa vasorum neovascularization, and mechanisms of plaque rupture are systematically evaluated. In the final thrombosis section, focal and circulating tissue factor associated with apoptotic macrophages and circulatory monocytes is examined, closing the link between inflammation, plaque rupture, and blood thrombogenicity.

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Section: Plaque Rupturementioning

confidence: 99%

Atherothrombosis and High-Risk Plaque

Fuster

Moreno

Fayad

et al. 2005

Journal of the American College of Cardiology

682

433

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“…observed with hypertension and early heart failure (13,14). The result is a weaker heart with greater internal work due to increased fibrosis (8,(14)(15)(16)(17).…”

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confidence: 99%

Exercise training attenuates age‐induced elevation in Bax/Bcl‐2 ratio, apoptosis, and remodeling in the rat heart

Kwak¹,

Song

Lawler³

2006

FASEB j.

146

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Aging is characterized by loss of myocytes, remodeling, and impaired contractile function in the heart. The rate of programmed cell death, or "apoptosis," in the left ventricle increases with age, and contributes to a 30% reduction in myocytes. Aging may preferentially target the Bcl-2 pathway of apoptosis in the heart. Exercise can protect cardiac function of the aging heart, although the mechanisms are poorly understood. We tested the hypothesis that 12 wk of exercise training would attenuate age-induced increases in remodeling, apoptosis, and Bax/Bcl-2 ratio in rat left ventricle. We found that exercise training provided significant protection against loss of cardiac myocytes, reduction in number of myonuclei, reactive hypertrophy of remaining myocytes, and increased connective tissue in left ventricle of the aging rat heart. Exercise training significantly attenuated age-induced increases of apoptosis in the left ventricle, as indicated by lower DNA fragmentation, TUNEL-positive staining, and caspase-3 cleavage, when compared with left ventricles from the age-matched sedentary group. Further, exercise training in the aging reduced caspase-9 levels and Bax/Bcl-2 ratio by lowering Bax protein expression while increasing Bcl-2 levels. These are the first data to demonstrate protective effects of endurance exercise training against elevated apoptosis and remodeling in the aging heart.

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“…Zhao et al (22) found that MMP-9 is overexpressed in the myocardium of patients with RHD congestive HF. Most of the studies concerning MMP-9 in HF, such as studies by Abou-Raya et al (23) Collier et al (24) and Morishita et al (25), suggest that active myocardial remodeling is associated with increased MMP-9 concentrations (10).…”

Section: Discussionmentioning

confidence: 99%

Matrix metalloproteinase‑9 in pediatric rheumatic heart disease with and without heart failure

et al. 2020

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In cardiovascular disorders, the myocardium may be subjected to the breakdown and remodeling of collagen by metalloproteinase-9 (MMP-9). We hypothesized that the serum MMP-9 concentration may be elevated in pediatric patients with rheumatic heart disease (RHD) and heart failure (HF), and its level can be correlated with the HF severity. Thus, in the present study, we aimed to evaluate the sensitivity and accuracy of MMP-9 to predict HF in children with RHD and to determine its effectiveness as an indicator of the degree of HF. This study included 98 consecutive children admitted to the

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71 Cardiac matrix remodelling in congestive heart failure: the role of matrix metalloproteinase (MMPs)

Cited by 6 publications

References 0 publications

Atherothrombosis and High-Risk Plaque

Atherothrombosis and High-Risk Plaque

Exercise training attenuates age‐induced elevation in Bax/Bcl‐2 ratio, apoptosis, and remodeling in the rat heart

Matrix metalloproteinase‑9 in pediatric rheumatic heart disease with and without heart failure

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