Heart failure is the number one reason for hospital admission and cardiac injury is the underlying etiology for 70% of heart failure cases. Despite improvements made in cardiovascular therapy, patient mortality is 42% at 5 years after hospitalization for heart failure. Following cardiac injury, necrosis of cardiomyocytes within the injured area elicits intense inflammation, and ultimately leads to replacement of dead cells with an extracellular matrix (ECM)-rich scar. Impaired suppression of inflammation and excessive accumulation of ECM proteins, such as collagen, in the interstitial and perivascular space result in stiffness of the left ventricle, thus contributing to the pathogenesis of heart failure.
Multiple preclinical and clinical trials have attempted to stimulate beneficial remodelling and decrease risk of heart failure in high-risk patient and while great strides have been made, there is much that still needs to be understood. Our understanding of the molecular mechanisms that determine what is beneficial versus adverse remodelling is needed in order to improve current therapies. The main objective of this Special Issue is to showcase manuscripts that have both a strong basic research background and a clear translational potential in the area of cardiac injury and disease. We encourage manuscript submissions that identify possible mechanisms for the prevention of progression of heart failure and/or for myocardial repair and regeneration in order to improve cardiovascular pathophysiology. This includes those studying regulation of coronary artery disease, cardiac remodeling (ischemic and non-ischemic), heart failure, hypertension, and cardiorenal syndrome.
Define the scope of the Research Topic, listing specific themes you would like contributors to address. Indicate the types of manuscripts you are interested in.
• Regulation of the inflammatory response in cardiovascular disease
• Novel models for testing hypothesis and treatments (e.g. 2D and 3D culture)
• Regulation and modulation of cardiac fibrosis and fibroblasts
• Molecular mediators of cardiac wound healing such as resolvins
We welcome all types of manuscripts, including: original basic science reports, review articles, methodology papers, translational research, and clinical studies.
Heart failure is the number one reason for hospital admission and cardiac injury is the underlying etiology for 70% of heart failure cases. Despite improvements made in cardiovascular therapy, patient mortality is 42% at 5 years after hospitalization for heart failure. Following cardiac injury, necrosis of cardiomyocytes within the injured area elicits intense inflammation, and ultimately leads to replacement of dead cells with an extracellular matrix (ECM)-rich scar. Impaired suppression of inflammation and excessive accumulation of ECM proteins, such as collagen, in the interstitial and perivascular space result in stiffness of the left ventricle, thus contributing to the pathogenesis of heart failure.
Multiple preclinical and clinical trials have attempted to stimulate beneficial remodelling and decrease risk of heart failure in high-risk patient and while great strides have been made, there is much that still needs to be understood. Our understanding of the molecular mechanisms that determine what is beneficial versus adverse remodelling is needed in order to improve current therapies. The main objective of this Special Issue is to showcase manuscripts that have both a strong basic research background and a clear translational potential in the area of cardiac injury and disease. We encourage manuscript submissions that identify possible mechanisms for the prevention of progression of heart failure and/or for myocardial repair and regeneration in order to improve cardiovascular pathophysiology. This includes those studying regulation of coronary artery disease, cardiac remodeling (ischemic and non-ischemic), heart failure, hypertension, and cardiorenal syndrome.
Define the scope of the Research Topic, listing specific themes you would like contributors to address. Indicate the types of manuscripts you are interested in.
• Regulation of the inflammatory response in cardiovascular disease
• Novel models for testing hypothesis and treatments (e.g. 2D and 3D culture)
• Regulation and modulation of cardiac fibrosis and fibroblasts
• Molecular mediators of cardiac wound healing such as resolvins
We welcome all types of manuscripts, including: original basic science reports, review articles, methodology papers, translational research, and clinical studies.
