Cardiac fibrosis is associated with heart dysfunction, which is the number one cause of death worldwide. Myocardial fibrosis is a pathophysiological response to tissue injury and is necessary for remodeling and healing. However, excessive fibrosis disrupts normal cardiac architecture and results in impaired ventricular function leading to sudden death and progressive heart failure.
The pathogenesis of cardiac fibrosis is generally characterized by excessive production rather than degradation of extracellular matrix (ECM), leading to disruption of myocardial excitation-contraction coupling and ultimately to systolic and diastolic dysfunction. The current literature describes two type of fibrosis in the heart: replacement fibrosis, which takes over post-ischemic injury in the myocardium or reactive fibrosis that occurs in absence of myocytes death through excessive extracellular matrix production. Myocardial fibrosis is not only a hallmark of cardiac injury but is commonly found in the aged heart as well as in cardiomyopathies induced by chemotherapy, radiotherapy, alcohol and autoimmune diseases. In addition, it has recently been shown that cardiac fibrosis is occurring in athletes as well as congenital and pediatric heart disease.
Depending on the classification of fibrosis (replacement vs. reactive) and the pathology leading to its development, the therapy might be different in terms of molecular target, duration or even timing of delivery for each intervention, but there is currently a gap in the literature exploring these differences. The myofibroblasts represent one of the potential therapeutic target because of their essential role in scar tissue formation, however the lack of a cell specific marker makes the field of cardiac fibrosis particularly challenging to investigate. Furthermore, there is urgency to find new circulating biomarkers and imaging methods to better quantify the extent of myocardial fibrosis and monitor treatment efficiency.
For this Research Topic, we welcome investigators to submit original research articles as well as review articles that will contribute to the field of Cardiac fibrosis. We welcome basic mechanistic studies in preclinical models as well as clinical studies focusing in understanding the pathophysiology, specific therapies targeting cardiac fibrosis and their outcomes.
We are particularly interested to the following topics:
- Preclinical studies using animal models of either replacement or reactive fibrosis, including lineage tracing of the cells involved in scar tissue formation, single cell sequencing, impaired Ca2+ signaling in cardiomyocytes
- New therapeutic approaches to prevent, reduce or revert cardiac fibrosis
- Circulating biomarkers of cardiac fibrosis
- New imaging methods to quantify cardiac fibrosis
- Cardiac fibrosis in cardiomyopathies induced by chemotherapy, radiotherapy or alcohol
- Role of myofibroblasts in cardiac physiology and heart disease
- Cardiac fibrosis in athletes and congenital/pediatric heart disease
- Cardiac fibrosis in autoimmune diseases
Cardiac fibrosis is associated with heart dysfunction, which is the number one cause of death worldwide. Myocardial fibrosis is a pathophysiological response to tissue injury and is necessary for remodeling and healing. However, excessive fibrosis disrupts normal cardiac architecture and results in impaired ventricular function leading to sudden death and progressive heart failure.
The pathogenesis of cardiac fibrosis is generally characterized by excessive production rather than degradation of extracellular matrix (ECM), leading to disruption of myocardial excitation-contraction coupling and ultimately to systolic and diastolic dysfunction. The current literature describes two type of fibrosis in the heart: replacement fibrosis, which takes over post-ischemic injury in the myocardium or reactive fibrosis that occurs in absence of myocytes death through excessive extracellular matrix production. Myocardial fibrosis is not only a hallmark of cardiac injury but is commonly found in the aged heart as well as in cardiomyopathies induced by chemotherapy, radiotherapy, alcohol and autoimmune diseases. In addition, it has recently been shown that cardiac fibrosis is occurring in athletes as well as congenital and pediatric heart disease.
Depending on the classification of fibrosis (replacement vs. reactive) and the pathology leading to its development, the therapy might be different in terms of molecular target, duration or even timing of delivery for each intervention, but there is currently a gap in the literature exploring these differences. The myofibroblasts represent one of the potential therapeutic target because of their essential role in scar tissue formation, however the lack of a cell specific marker makes the field of cardiac fibrosis particularly challenging to investigate. Furthermore, there is urgency to find new circulating biomarkers and imaging methods to better quantify the extent of myocardial fibrosis and monitor treatment efficiency.
For this Research Topic, we welcome investigators to submit original research articles as well as review articles that will contribute to the field of Cardiac fibrosis. We welcome basic mechanistic studies in preclinical models as well as clinical studies focusing in understanding the pathophysiology, specific therapies targeting cardiac fibrosis and their outcomes.
We are particularly interested to the following topics:
- Preclinical studies using animal models of either replacement or reactive fibrosis, including lineage tracing of the cells involved in scar tissue formation, single cell sequencing, impaired Ca2+ signaling in cardiomyocytes
- New therapeutic approaches to prevent, reduce or revert cardiac fibrosis
- Circulating biomarkers of cardiac fibrosis
- New imaging methods to quantify cardiac fibrosis
- Cardiac fibrosis in cardiomyopathies induced by chemotherapy, radiotherapy or alcohol
- Role of myofibroblasts in cardiac physiology and heart disease
- Cardiac fibrosis in athletes and congenital/pediatric heart disease
- Cardiac fibrosis in autoimmune diseases