We are analyzing https://link.springer.com/article/10.1007/s00441-016-2431-9.

Title:
Cardiac fibrosis in myocardial infarction—from repair and remodeling to regeneration | Cell and Tissue Research
Description:
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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Keywords {🔍}

cardiac, pubmed, article, google, scholar, cas, fibroblasts, fibrosis, cell, cells, reprogramming, heart, central, remodeling, myofibroblasts, cardiomyocytes, myocardial, signaling, tgfβ, direct, factor, res, myocardium, infarction, response, inhibition, area, tissue, fibroblast, regeneration, factors, ventricular, role, cardiol, frangogiannis, growth, receptor, collagen, ecm, expression, mol, function, reactive, proteins, circ, fibrotic, scar, injury, type, effects,

Topics {✒️}

deleterious ang-ii-independent actions α-smooth muscle actin tissue renin-angiotensin-aldosterone systems transforming growth factor-β1 virpi talman tgf-β-induced excessive production platelet-derived growth factor eda-fn extra-domain-a smad3-dependent tgf-β signaling at1 receptor-mediated tgf-β distinct context-dependent mechanisms advanced glycation end-products cyclic guanosine monophosphate article download pdf enhancing anti-fibrotic signaling pressure-overload-induced fibrosis exhibit anti-fibrotic properties mineralocorticoid/aldosterone receptor antagonists perivascular gli1+ mesenchymal-stem-cell therapeutic cardiac-targeted delivery ang ii-independent manner article talman exhibit anti-fibrotic effects central signaling molecule pro-fibrotic factors initiating transforming growth factor exhibit anti-remodeling properties lox-catalyzed cross-linking post-infarction cardiac regeneration potent pro-fibrotic mediator ang ii-induced fibrosis injury-induced organ fibrosis latent tgf-β1 complex α-sma-expressing myofibroblasts ang ii-independent mechanism fibroblast-myocyte electrotonic coupling angiotensin ii-infused mice secrete pro-fibrotic factors tgf-β-activated kinase nicotine-induced atrial remodelling activating cgmp-mediated pathways pressure-overloaded adult hearts post-mi inflammatory reaction central cell type angiotensin ii-dependent hypertension efficient anti-fibrotic drugs post-mi remodeling correlating β2 receptor-selective antagonists controlling post-mi fibrosis stress-inducible secreted glycoproteins

Questions {❓}

Kohan DE, Cleland JG, Rubin LJ, Theodorescu D, Barton M (2012) Clinical trials with endothelin receptor antagonists: what went wrong and where can we improve?
Kohl P, Gourdie RG (2014) Fibroblast-myocyte electrotonic coupling: does it occur in native cardiac tissue?
Rodriguez-Pascual F, Busnadiego O, Gonzalez-Santamaria J (2014) The profibrotic role of endothelin-1: is the door still open for the treatment of fibrotic diseases?

Schema {🗺️}

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      headline:Cardiac fibrosis in myocardial infarction—from repair and remodeling to regeneration
      description: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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