Fibrotic diseases cause annually more than 800,000 deaths worldwide, where of the majority accounts for cardiovascular fibrosis. Commonly, cardiovascular fibrosis refers to the development of scar tissues in the injured heart and blood vessels due to an aberrant wound-healing response to injury or insult, which arises from enhanced inflammatory processes, uncontrolled cell proliferation and excessive oxidative stress. Established cardiovascular fibrosis is a hallmark of many cardiovascular diseases such as atherosclerosis, coronary artery diseases, hypertension, dilated cardiomyopathy, atrial fibrillation, heart failure, pulmonary hypertension, and diabetic cardiovascular complications. Fibrotic change is a key contributor to cardiovascular stiffness and remodeling, ultimately leading to cardiac and vascular dysfunction and other cardiovascular disorders. Unfortunately, current effective therapies for cardiovascular fibrosis-related diseases are still lacking.
Cardiovascular fibrosis is characterized by a reduction in parenchymal cells and increase in interstitial cells, which maintain the relative integrity of the cardiovascular system. Recruitment of inflammatory immune cells and activation of the renin-angiotensin system play critical roles in the early phase of cardiovascular fibrosis, followed by fibroblast activation and myofibroblast differentiation leading to the production and deposition of extracellular matrix proteins. Angiotensin II, endothelin-1, TGF-ß1, CTGF, MMPs/TIMPs and proinflammatory factors are well-known contributors of cardiovascular fibrosis. Notably, emerging evidence highlights the mechanistic roles of noncoding RNAs (ncRNAs) in the pathophysiology and manifestation of cardiovascular fibrosis and related diseases.
In this Research Topic, we focus on the pathophysiology and the underlying mechanisms of cardiovascular fibrosis and development of effective interventions for fibrotic progression in cardiovascular diseases. We also encourage the review and original manuscript that cover or demonstrate the latest advances in the regulatory roles and mechanisms of ncRNAs in cardiovascular fibrosis and related diseases. Clinical research for early diagnosis and prognosis of cardiovascular fibrosis will also be welcomed.
Areas to be covered in this research topic may include, but are not limited to:
1) An update or novel knowledge on the pathophysiology and underlying cellular and molecular mechanisms of cardiovascular fibrosis and related diseases.
2) Novel biological functions and signaling transduction of ncRNAs in cardiovascular fibrosis and related diseases.
3) The mRNA-miRNA-lncRNA or mRNA-miRNA-circRNA regulatory network in fibrosis-related cardiovascular diseases.
4) Novel therapeutic strategies for cardiovascular fibrosis: pharmacological therapy, gene therapy, cell therapy, and extracellular vesicles, etc.
5) Clinical device examinations or biomarkers for early diagnosis and prognosis of cardiovascular fibrosis.
Fibrotic diseases cause annually more than 800,000 deaths worldwide, where of the majority accounts for cardiovascular fibrosis. Commonly, cardiovascular fibrosis refers to the development of scar tissues in the injured heart and blood vessels due to an aberrant wound-healing response to injury or insult, which arises from enhanced inflammatory processes, uncontrolled cell proliferation and excessive oxidative stress. Established cardiovascular fibrosis is a hallmark of many cardiovascular diseases such as atherosclerosis, coronary artery diseases, hypertension, dilated cardiomyopathy, atrial fibrillation, heart failure, pulmonary hypertension, and diabetic cardiovascular complications. Fibrotic change is a key contributor to cardiovascular stiffness and remodeling, ultimately leading to cardiac and vascular dysfunction and other cardiovascular disorders. Unfortunately, current effective therapies for cardiovascular fibrosis-related diseases are still lacking.
Cardiovascular fibrosis is characterized by a reduction in parenchymal cells and increase in interstitial cells, which maintain the relative integrity of the cardiovascular system. Recruitment of inflammatory immune cells and activation of the renin-angiotensin system play critical roles in the early phase of cardiovascular fibrosis, followed by fibroblast activation and myofibroblast differentiation leading to the production and deposition of extracellular matrix proteins. Angiotensin II, endothelin-1, TGF-ß1, CTGF, MMPs/TIMPs and proinflammatory factors are well-known contributors of cardiovascular fibrosis. Notably, emerging evidence highlights the mechanistic roles of noncoding RNAs (ncRNAs) in the pathophysiology and manifestation of cardiovascular fibrosis and related diseases.
In this Research Topic, we focus on the pathophysiology and the underlying mechanisms of cardiovascular fibrosis and development of effective interventions for fibrotic progression in cardiovascular diseases. We also encourage the review and original manuscript that cover or demonstrate the latest advances in the regulatory roles and mechanisms of ncRNAs in cardiovascular fibrosis and related diseases. Clinical research for early diagnosis and prognosis of cardiovascular fibrosis will also be welcomed.
Areas to be covered in this research topic may include, but are not limited to:
1) An update or novel knowledge on the pathophysiology and underlying cellular and molecular mechanisms of cardiovascular fibrosis and related diseases.
2) Novel biological functions and signaling transduction of ncRNAs in cardiovascular fibrosis and related diseases.
3) The mRNA-miRNA-lncRNA or mRNA-miRNA-circRNA regulatory network in fibrosis-related cardiovascular diseases.
4) Novel therapeutic strategies for cardiovascular fibrosis: pharmacological therapy, gene therapy, cell therapy, and extracellular vesicles, etc.
5) Clinical device examinations or biomarkers for early diagnosis and prognosis of cardiovascular fibrosis.
