Cardiac fibrosis in myocardial infarction - from repair and remodeling to regeneration

Tutkimustuotos: ArtikkelijulkaisuKatsausartikkeliTieteellinenvertaisarvioitu

Kuvaus

Ischemic cell death during a myocardial infarction leads to a multiphase reparative response in which the damaged tissue is replaced with a fibrotic scar produced by fibroblasts and myofibroblasts. This also induces geometrical, biomechanical, and biochemical changes in the uninjured ventricular wall eliciting a reactive remodeling process that includes interstitial and perivascular fibrosis. Although the initial reparative fibrosis is crucial for preventing rupture of the ventricular wall, an exaggerated fibrotic response and reactive fibrosis outside the injured area are detrimental as they lead to progressive impairment of cardiac function and eventually to heart failure. In this review, we summarize current knowledge of the mechanisms of both reparative and reactive cardiac fibrosis in response to myocardial infarction, discuss the potential of inducing cardiac regeneration through direct reprogramming of fibroblasts and myofibroblasts into cardiomyocytes, and review the currently available and potential future therapeutic strategies to inhibit cardiac fibrosis.
Alkuperäiskielienglanti
LehtiCell and Tissue Research
Vuosikerta365
Numero3
Sivut563-581
Sivumäärä19
ISSN0302-766X
DOI - pysyväislinkit
TilaJulkaistu - 1 syyskuuta 2016
OKM-julkaisutyyppiA2 Katsausartikkeli tieteellisessä aikakauslehdessä

Tieteenalat

  • 317 Farmasia

Lainaa tätä

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title = "Cardiac fibrosis in myocardial infarction - from repair and remodeling to regeneration",
abstract = "Ischemic cell death during a myocardial infarction leads to a multiphase reparative response in which the damaged tissue is replaced with a fibrotic scar produced by fibroblasts and myofibroblasts. This also induces geometrical, biomechanical, and biochemical changes in the uninjured ventricular wall eliciting a reactive remodeling process that includes interstitial and perivascular fibrosis. Although the initial reparative fibrosis is crucial for preventing rupture of the ventricular wall, an exaggerated fibrotic response and reactive fibrosis outside the injured area are detrimental as they lead to progressive impairment of cardiac function and eventually to heart failure. In this review, we summarize current knowledge of the mechanisms of both reparative and reactive cardiac fibrosis in response to myocardial infarction, discuss the potential of inducing cardiac regeneration through direct reprogramming of fibroblasts and myofibroblasts into cardiomyocytes, and review the currently available and potential future therapeutic strategies to inhibit cardiac fibrosis.",
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author = "Virpi Talman and Ruskoaho, {Heikki Juhani}",
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Cardiac fibrosis in myocardial infarction - from repair and remodeling to regeneration. / Talman, Virpi; Ruskoaho, Heikki Juhani.

julkaisussa: Cell and Tissue Research, Vuosikerta 365, Nro 3, 01.09.2016, s. 563-581.

Tutkimustuotos: ArtikkelijulkaisuKatsausartikkeliTieteellinenvertaisarvioitu

TY - JOUR

T1 - Cardiac fibrosis in myocardial infarction - from repair and remodeling to regeneration

AU - Talman, Virpi

AU - Ruskoaho, Heikki Juhani

PY - 2016/9/1

Y1 - 2016/9/1

N2 - Ischemic cell death during a myocardial infarction leads to a multiphase reparative response in which the damaged tissue is replaced with a fibrotic scar produced by fibroblasts and myofibroblasts. This also induces geometrical, biomechanical, and biochemical changes in the uninjured ventricular wall eliciting a reactive remodeling process that includes interstitial and perivascular fibrosis. Although the initial reparative fibrosis is crucial for preventing rupture of the ventricular wall, an exaggerated fibrotic response and reactive fibrosis outside the injured area are detrimental as they lead to progressive impairment of cardiac function and eventually to heart failure. In this review, we summarize current knowledge of the mechanisms of both reparative and reactive cardiac fibrosis in response to myocardial infarction, discuss the potential of inducing cardiac regeneration through direct reprogramming of fibroblasts and myofibroblasts into cardiomyocytes, and review the currently available and potential future therapeutic strategies to inhibit cardiac fibrosis.

AB - Ischemic cell death during a myocardial infarction leads to a multiphase reparative response in which the damaged tissue is replaced with a fibrotic scar produced by fibroblasts and myofibroblasts. This also induces geometrical, biomechanical, and biochemical changes in the uninjured ventricular wall eliciting a reactive remodeling process that includes interstitial and perivascular fibrosis. Although the initial reparative fibrosis is crucial for preventing rupture of the ventricular wall, an exaggerated fibrotic response and reactive fibrosis outside the injured area are detrimental as they lead to progressive impairment of cardiac function and eventually to heart failure. In this review, we summarize current knowledge of the mechanisms of both reparative and reactive cardiac fibrosis in response to myocardial infarction, discuss the potential of inducing cardiac regeneration through direct reprogramming of fibroblasts and myofibroblasts into cardiomyocytes, and review the currently available and potential future therapeutic strategies to inhibit cardiac fibrosis.

KW - 317 Pharmacy

U2 - 10.1007/s00441-016-2431-9

DO - 10.1007/s00441-016-2431-9

M3 - Review Article

VL - 365

SP - 563

EP - 581

JO - Cell and Tissue Research

JF - Cell and Tissue Research

SN - 0302-766X

IS - 3

ER -