Conţinutul numărului revistei |
Articolul precedent |
Articolul urmator |
250 0 |
Căutarea după subiecte similare conform CZU |
616.127-002.17-005.8-092.18 (1) |
Patologia sistemului circulator, a vaselor sanguine. Tulburări cardiovasculare (978) |
SM ISO690:2012 LECA, Magdalena. Post-infarct fibrosis of the myocardium: mechanisms and predictors. In: Revista de Ştiinţe ale Sănătăţii din Moldova, 2022, nr. 3 An.1(29), p. 40. ISSN 2345-1467. |
EXPORT metadate: Google Scholar Crossref CERIF DataCite Dublin Core |
Revista de Ştiinţe ale Sănătăţii din Moldova | ||||||
Numărul 3 An.1(29) / 2022 / ISSN 2345-1467 | ||||||
|
||||||
CZU: 616.127-002.17-005.8-092.18 | ||||||
Pag. 40-40 | ||||||
|
||||||
Descarcă PDF | ||||||
Rezumat | ||||||
Background. AMI is a notable cause of heart failure, which is associated by the development of post-infarction myocardial fibrosis, and the cellular effectors and molecular pathways involved are important predictors and therapeutic targets. Objective of the study. To evaluate the mediators of the pathogenic interface including the mechanisms of post-infarct cardiac fibrosis triggering and progression. Methods and materials: Scientific articles regarding the pathophysiological arrangements of myocardial post-infarct fibrosis and inherent predictors, as well as the diagnostic methods (biomarkers, EchoCG, MRI) and potential pathogenic treatment schemes have been analyzed. Results. Post-infarction fibrosis, as a pattern of remodeling of the extracellular matrix, is triggered by the phenomenon of myocardial necrosis and associated events. Inflammatory cytokines and chemokines, reactive oxygen species, mast cell-derived proteases, endothelin-1, renin-angiotensin-aldosterone system, extracellular matrix proteins, and growth factors (e.g., TGF-β and PDGF) are some of the best studied mediators involved in cardiac fibrosis. The arsenal of diagnostic methods includes: serum markers of collagen turnover, galectin-3, EcoCG exam inclusive with Speckle Tracking maneuver, MRI. Conclusion. Post-infarction myocardial fibrosis is based on the synthesis of fibrillar collagen type I and III by fibroblasts and myofibroblasts, which is detrimental for the lusitropic function of the heart, and the highlighting of algorithm of specific markers has connotations |
||||||
Cuvinte-cheie post-infarction cardiac fibrosis, Galectin-3, TGF-β, PDGF, extracellular matrix, predictors, fibroză cardiacă post-infarct, galectina-3, TGF-β, PDGF, matrice extracelulară, predictori |
||||||
|