Matrix metalloproteinase-3 gene polymorphism and dilatative pathology of ascending thoracic aorta

Lesauskaitė, Vaiva; Šinkūnaitė, Giedrė; Benetis, Rimantas; Grabauskas, Vilius Jonas; Vaškelytė, Jolanta Justina; Smalinskienė, Alina; Šimonytė, Sandrita; Jarienė, Giedrė; Tatarūnas, Vacis; Klumbienė, Jūratė; Petkevičienė, Janina; Kinduris, Šarūnas; Giedraitis, Saulius; Sakalauskas, Juozas; Bolys, Ramūnas; Širvinskas, Edmundas; Lenkutis, Tadas; Pangonytė, Dalia

doi:10.3390/medicina44050050

Cited by 24 publications

(14 citation statements)

References 31 publications

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“…The frequency of 5A allele did not differ significantly between both groups and was 0.506 and 0.514, respectively. Male carriers of 5A/5A genotype were significantly younger compared with those with the 6A/6A genotype [29].…”

Section: Mmp-pathwaysmentioning

confidence: 92%

Genetic contribution in sporadic thoracic aortic aneurysm? Emerging evidence of genetic variants related to TLR-4-mediated signaling pathway as risk determinants

Balistreri

2015

Vascular Pharmacology

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Keywords:Sporadic thoracic aortic aneurysms (TAA) and dissections Genetic variants Biomarkers Targets for new personalized therapeutic treatments Sporadic thoracic aortic aneurysms (TAA) and dissections are one of the major causes of morbidity and mortality worldwide, especially in those older than 65 years. The presentation of TAA is varied and often silent. Thus, sporadic TAA detection is often fortuitous, with identification occurring during a routine physical examination or during an unrelated medical evaluation. Once suspected, confirmation by imaging clinical approaches is needed to allow the choose of the unique treatments for TAA, namely the surgery procedures, including elective surgery or endovascular repair before the onset of catastrophic and fatal complications, such as dissection or rupture. At present, there are no biomarkers available to identify TAAs before visible symptoms. However, recent progresses in understanding of molecular and cellular mechanisms involved in the patho-physiology of sporadic TAA are suggesting different molecular pathways and their genetic variants as potential biomarkers, which might be applied into TAA clinical practice in the near future. Here, we report literature evidence on some disease pathways and their genetic variants on TAA susceptibility and compliances, and their translation as promising TAA preventive and prognostic biomarkers and targets for new personalized therapeutic treatments.

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Section: Mmp-pathwaysmentioning

confidence: 92%

Genetic contribution in sporadic thoracic aortic aneurysm? Emerging evidence of genetic variants related to TLR-4-mediated signaling pathway as risk determinants

Balistreri

2015

Vascular Pharmacology

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“…In this way, MMP-3 is crucial to the connective tissue remodeling process; it is involved in the turnover of numerous ecM components (18).…”

Section: Matrix Metalloproteinase-3mentioning

confidence: 99%

MMP-3 polymorphism: Genetic marker in pathological processes (Review)

2010

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Abstract. Matrix metalloproteinases (MMPs) are a family of zinc-dependent endopeptidases that are collectively capable of cleaving virtually all extracellular matrix (ecM) substrates and play an important role in diverse physiological and pathological processes. The activity of MMPs is controlled at multiple levels, and the transcriptional regulation of MMPs appears to represent a necessary step in its regulation. MMP-3 is a key member of the MMP family with broad substrate specificity, and is crucial to the connective tissue remodeling process. it is also involved in the turnover of the numerous ecM components. a common functional promoter polymorphism of MMP-3, 5a/6a, affects its activity and has been associated with various diseases. This polymorphism may be used as a genetic marker for certain pathologies to identify individual susceptibility. This review discusses various topics related to MMP-3 in pathological processes, with a focus on the 5a/6a polymorphism. Contents1. introduction 2. Matrix metalloproteinase-3 3. 5a/6a polymorphism of MMP-3 4. Pathological processes and the MMP-3 5a/6a polymorphism 5. Haplotype influence IntroductionThe evidence that individual characteristics play an important role in physiological and pathological processes has resulted in the targeted study of genetic polymorphisms in the clinical setting. in this context, mediators that degrade the extracellular matrix (ecM), such as matrix metalloproteinases (MMPs), are highlighted in studies involving inflammatory and degenerative diseases, and principally the prognosis and metastasis of cancer.degradation of the ecM is essential in many physiological processes, such as during development, growth and repair of tissue, and the microenvironment plays a central role in controlling both normal and transformed cell functions, as well as normal tissue integrity (1).MMPs are a pivotal family of zinc enzymes responsible for the degradation of ecM components, including basement membrane collagen, interstitial collagen, fibronectin and various proteoglycans, during normal remodeling and repair processes in development and inflammation. MMPs are also peptidase enzymes responsible for clotting factors, lipoproteins, latent growth factors and chemotactic and cell adhesion molecules (2,3). in this way, MMPs play a key role in the physiologic remodeling of tissues, including embryogenesis and tissue morphogenesis, angiogenesis, cell migration, proliferation, apoptosis, alteration of cell motility, effects on the immune system, wound repair and the inflammatory response (4).MMPs are a family of more than 25 enzymes. The expression of most MMPs is normally low in tissues and is induced when remodeling of the ecM is required. MMP gene expression is regulated primarily at the transcriptional level, but there is also evidence of the modulation of mrna stability in response to growth factors and cytokines (5). The promoter region of inducible MMP genes (i.e., MMP-3) shows remarkable conservation of regulatory elements, and their expression is induced ...

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“…A key member of the MMP family, MMP3 is known to lyse basal membrane collagen and induce the synthesis of other MMP. MMP3 polymorphism is due to a variation in the number of adenosines located at position 1171 relative to the transcription start site, resulting in one allele having five adenosines (5A) and the other allele having six adenosines (6A) [21][22][23]. The results of our observations, in addition to meta-analysis, revealed that the 6A/6A genotype and 6A allele was significantly associated with MMD susceptibility.…”

Section: Discussionmentioning

confidence: 55%

Association between matrix metalloproteinase-3 gene polymorphism and moyamoya disease

You

2015

Journal of Clinical Neuroscience

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Matrix metalloproteinase-3 gene polymorphism and dilatative pathology of ascending thoracic aorta

Cited by 24 publications

References 31 publications

Genetic contribution in sporadic thoracic aortic aneurysm? Emerging evidence of genetic variants related to TLR-4-mediated signaling pathway as risk determinants

Genetic contribution in sporadic thoracic aortic aneurysm? Emerging evidence of genetic variants related to TLR-4-mediated signaling pathway as risk determinants

MMP-3 polymorphism: Genetic marker in pathological processes (Review)

Association between matrix metalloproteinase-3 gene polymorphism and moyamoya disease

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