Worldwide, cardiovascular diseases affects millions, cause serious economic burden and represent the number one cause of death. A broad range of pathological cardiac conditions are associated with myocardial tissue remodelling and fibrosis. Cardiac fibrosis reflects the exaggerated accumulation of extracellular matrix components, activation of stromal cell compartments in the tissue, followed by acute or chronic inflammatory responses. Progressive cardiac fibrosis has been recognized to cause life-threating arrhythmias. The development of life-saving therapeutic strategies and new medications requires extensive scientific efforts to understand the pathophysiology of pro-arrhythmogenic fibrosis, which is currently poorly understood. Understanding the cellular and molecular bases of cardiac fibrogenesis is crucial for identifying potential diagnostic and therapeutic targets in cardiovascular diseases.
The aim of this Research Topic is a wide-ranging overview of the current understanding of the mechanisms and consequences of myocardial fibrosis across diverse cardiovascular disorders.
In this Research Topic, we encourage submissions describing novel findings in the aetiology of myocardial fibrosis, potential mechanisms driving this process, cell-to-cell interactions, crosstalk of stromal cells with other cell types, cellular source of pathological cardiac myofibroblasts, and cellular diversity analysed with different single cell technology. We aim to receive submissions from studies which aspect myocardial fibrosis and studies answering the following: how and which aspect of myocardial fibrosis affects heart dysfunctions, novel animal and 3D models mimicking human cardiac pathology. We also put a high interest on studies presenting effective pre-clinical and clinical anti-fibrotic strategies.
Themes of interests include but are not limited to:
1) Cellular characteristic on single cell level.
2) Cell-to-cell interaction.
3) Crosstalk of stromal cells with other cell types.
4) Autophagy-fibrosis crosstalk in the fibrotic heart.
5) Molecular signalling controlling myocardial fibrosis on single cell level.
6) Aetiology of myocardial fibrosis, novel insights.
7) Fibrosis effects on heart dysfunction and potential treatment.
8) Fibrosis-triggered arrhythmias.
Worldwide, cardiovascular diseases affects millions, cause serious economic burden and represent the number one cause of death. A broad range of pathological cardiac conditions are associated with myocardial tissue remodelling and fibrosis. Cardiac fibrosis reflects the exaggerated accumulation of extracellular matrix components, activation of stromal cell compartments in the tissue, followed by acute or chronic inflammatory responses. Progressive cardiac fibrosis has been recognized to cause life-threating arrhythmias. The development of life-saving therapeutic strategies and new medications requires extensive scientific efforts to understand the pathophysiology of pro-arrhythmogenic fibrosis, which is currently poorly understood. Understanding the cellular and molecular bases of cardiac fibrogenesis is crucial for identifying potential diagnostic and therapeutic targets in cardiovascular diseases.
The aim of this Research Topic is a wide-ranging overview of the current understanding of the mechanisms and consequences of myocardial fibrosis across diverse cardiovascular disorders.
In this Research Topic, we encourage submissions describing novel findings in the aetiology of myocardial fibrosis, potential mechanisms driving this process, cell-to-cell interactions, crosstalk of stromal cells with other cell types, cellular source of pathological cardiac myofibroblasts, and cellular diversity analysed with different single cell technology. We aim to receive submissions from studies which aspect myocardial fibrosis and studies answering the following: how and which aspect of myocardial fibrosis affects heart dysfunctions, novel animal and 3D models mimicking human cardiac pathology. We also put a high interest on studies presenting effective pre-clinical and clinical anti-fibrotic strategies.
Themes of interests include but are not limited to:
1) Cellular characteristic on single cell level.
2) Cell-to-cell interaction.
3) Crosstalk of stromal cells with other cell types.
4) Autophagy-fibrosis crosstalk in the fibrotic heart.
5) Molecular signalling controlling myocardial fibrosis on single cell level.
6) Aetiology of myocardial fibrosis, novel insights.
7) Fibrosis effects on heart dysfunction and potential treatment.
8) Fibrosis-triggered arrhythmias.