The term cardiac fibrosis is used to describe the excessive expansion of the extracellular matrix (ECM) network that occurs in most pathological forms of heart disease. In conditions including myocardial infarction, hypertension, obesity, diabetes and aging, cardiac fibrosis is a hallmark of cardiac dysfunction and successive heart failure. In myocardial infarction cardiac fibrosis has a dual role since it plays an important reparative function preventing cardiac rupture but also induces a reactive remodeling process in the non-injured myocardial wall. In non-ischemic heart diseases, the excessive interstitial and perivascular deposition of ECM proteins may cause myocardial stiffness and dysfunction, leading eventually to heart failure. The severity of systolic and diastolic dysfunction, arrhythmias and adverse outcome depends on the extend of cardiac fibrosis. Considering the dual reparative/detrimental role of cardiac fibrosis, targeting fibrotic remodeling is challenging and, to date, no effective anti-fibrotic strategies are available. A beneficial therapeutic approach against cardiac fibrosis should aim to blunt excessive fibrotic responses while safely preserve its reparative role.
The main cellular effectors in cardiac fibrosis are fibroblasts - interstitial secreting cells that expand upon myocardial injury. Several other cardiac cell types such as cardiomyocytes, endothelial cells, pericytes, macrophages, lymphocytes and mast cells, however, seem to be involved in the fibrotic process; their role in cardiac fibrosis is still unknown. Understanding the cell-specific contribution of cardiac cells to the development of the fibrotic process while dissecting novel molecular pathways that may serve as anti-fibrotic targets has been the goal of most of the studies over the last years.
Within this Research Topic, we aim to collect articles (original research, review and methodological manuscripts) representing the state of the art and future perspectives in basic and translational cardiac fibrosis research. Areas of interest include but are not limited to:
• Molecular and cellular mechanisms involved in the cardiac fibrotic process in both ischemic and non-ischemic conditions (myocardial infarction, hypertension, aging, obesity, diabetes, genetic diseases.
• Cell-specific contribution of myocardial and non-myocardial cells to the pathogenesis of cardiac fibrosis.
• In vivo (animal models) in in vitro (organoids, tissue culture, AI-based) models recapitulating cardiac fibrosis for pharmacological research and drug discovery.
• Preclinical and/or clinical studies aimed to test potential novel therapeutic targets against cardiac fibrosis.
• Novel diagnostic or prognostic tools for cardiac fibrosis (molecular imaging, circulating biomarkers including proteomics and metabolomics).
The term cardiac fibrosis is used to describe the excessive expansion of the extracellular matrix (ECM) network that occurs in most pathological forms of heart disease. In conditions including myocardial infarction, hypertension, obesity, diabetes and aging, cardiac fibrosis is a hallmark of cardiac dysfunction and successive heart failure. In myocardial infarction cardiac fibrosis has a dual role since it plays an important reparative function preventing cardiac rupture but also induces a reactive remodeling process in the non-injured myocardial wall. In non-ischemic heart diseases, the excessive interstitial and perivascular deposition of ECM proteins may cause myocardial stiffness and dysfunction, leading eventually to heart failure. The severity of systolic and diastolic dysfunction, arrhythmias and adverse outcome depends on the extend of cardiac fibrosis. Considering the dual reparative/detrimental role of cardiac fibrosis, targeting fibrotic remodeling is challenging and, to date, no effective anti-fibrotic strategies are available. A beneficial therapeutic approach against cardiac fibrosis should aim to blunt excessive fibrotic responses while safely preserve its reparative role.
The main cellular effectors in cardiac fibrosis are fibroblasts - interstitial secreting cells that expand upon myocardial injury. Several other cardiac cell types such as cardiomyocytes, endothelial cells, pericytes, macrophages, lymphocytes and mast cells, however, seem to be involved in the fibrotic process; their role in cardiac fibrosis is still unknown. Understanding the cell-specific contribution of cardiac cells to the development of the fibrotic process while dissecting novel molecular pathways that may serve as anti-fibrotic targets has been the goal of most of the studies over the last years.
Within this Research Topic, we aim to collect articles (original research, review and methodological manuscripts) representing the state of the art and future perspectives in basic and translational cardiac fibrosis research. Areas of interest include but are not limited to:
• Molecular and cellular mechanisms involved in the cardiac fibrotic process in both ischemic and non-ischemic conditions (myocardial infarction, hypertension, aging, obesity, diabetes, genetic diseases.
• Cell-specific contribution of myocardial and non-myocardial cells to the pathogenesis of cardiac fibrosis.
• In vivo (animal models) in in vitro (organoids, tissue culture, AI-based) models recapitulating cardiac fibrosis for pharmacological research and drug discovery.
• Preclinical and/or clinical studies aimed to test potential novel therapeutic targets against cardiac fibrosis.
• Novel diagnostic or prognostic tools for cardiac fibrosis (molecular imaging, circulating biomarkers including proteomics and metabolomics).
