Stimulation of the epicardium as a source of myocardial repair: from experiment to clinical practice

Mortality from myocardial infarction and its complications — heart rhythm disturbances, myocardial remodeling with subsequent development of congestive heart failure — occupies a leading place in the world. Activation of the epicardium is being actively studied as one of the ways to prevent cardiac remodeling. The method is based on the ability of embryonic epicardial cells to undergo epithelial-mesenchymal transformation, as a result of which the resulting epicardial-derived cells give rise to various cytological lines — cardiac fibroblasts, smooth muscle cells of the vascular wall, adipocytes and cardiomyocytes. In the postnatal period, this regenerative potential is absent. Currently, various methods have been developed to activate the reparative potential of the epicardium using options for genetic reprogramming of epicardial cells using viral vectors, exposure to paracrine factors involved in the formation of the heart and its structures — transcription factors GATA4, GATA6, thymosin-β4, introduction of embryonic stem cells or induced pluripotent stem cells in tissue-engineered constructs, activation of fibroblast growth factors ( FGF ), and platelet-derived growth factor ( PDGF ). These methods are being actively studied in experimental models of myocardial infarction and have shown their high efficiency in vitro. The results of transplantation of tissue-engineered structures during coronary artery bypass surgery in patients with severe post-infarction heart failure show promise in terms of slowing down myocardial remodeling.

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Publication Details

Journal
Pediatrician (St Petersburg)
Published
2024-11-20
DOI
https://doi.org/10.17816/ped15571-80
Primary Topic
Congenital heart defects research
Type
article
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article

Stimulation of the epicardium as a source of myocardial repair: from experiment to clinical practice

Yana E. Bulavko, Е.В. Тимофеев
Pediatrician (St Petersburg)
Congenital heart defects research
article

Stimulation of the epicardium as a source of myocardial repair: from experiment to clinical practice

Yana E. Bulavko, Е.В. Тимофеев
article en

Abstract

Mortality from myocardial infarction and its complications — heart rhythm disturbances, myocardial remodeling with subsequent development of congestive heart failure — occupies a leading place in the world. Activation of the epicardium is being actively studied as one of the ways to prevent cardiac remodeling. The method is based on the ability of embryonic epicardial cells to undergo epithelial-mesenchymal transformation, as a result of which the resulting epicardial-derived cells give rise to various cytological lines — cardiac fibroblasts, smooth muscle cells of the vascular wall, adipocytes and cardiomyocytes. In the postnatal period, this regenerative potential is absent. Currently, various methods have been developed to activate the reparative potential of the epicardium using options for genetic reprogramming of epicardial cells using viral vectors, exposure to paracrine factors involved in the formation of the heart and its structures — transcription factors GATA4, GATA6, thymosin-β4, introduction of embryonic stem cells or induced pluripotent stem cells in tissue-engineered constructs, activation of fibroblast growth factors ( FGF ), and platelet-derived growth factor ( PDGF ). These methods are being actively studied in experimental models of myocardial infarction and have shown their high efficiency in vitro. The results of transplantation of tissue-engineered structures during coronary artery bypass surgery in patients with severe post-infarction heart failure show promise in terms of slowing down myocardial remodeling.

Pediatrician (St Petersburg)Vol. 15(5)
Saint Petersburg State Pediatric Medical University (RU)
Openalex Percentile: Top 78%
Congenital heart defects research
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Stimulation of the epicardium as a source of myocardial repair: from experiment to clinical practice — Yana E. Bulavko, Е.В. Тимофеев · Pediatrician (St Petersburg) (2024) | TGRS Research Map | TGRS