Special Issue "Cardiac Fibrosis: From Pathogenesis to Targeted Therapies"
Deadline for manuscript submissions: closed (15 October 2023) | Viewed by 1131
Interests: heart disease; cell death; hypertrophy; fibrosis
Despite the recent advances in diagnosis and therapies, cardiovascular diseases remain the leading cause of death worldwide. Many types of cardiovascular diseases are associated with cardiac fibrosis, which is characterized by an increase in the extracellular matrix in the heart. Extracellular matrix proteins are primarily produced by cardiac fibroblasts. In response to pathological injury, quiescent fibroblasts become active and differentiate into myofibroblasts, leading to the synthesis and secretion of extracellular matrix proteins. The secreted extracellular matrix proteins may help to maintain the structural integrity of the heart after injuries. However, prolonged fibrosis interferes with myocardial contraction and relaxation, resulting in reduced compliance, cardiac dysfunction, and eventually heart failure. At present, there is no FDA-approved drug that specifically targets cardiac fibrosis. Understanding the molecular and cellular mechanisms of cardiac fibrosis could reveal novel signaling pathways that can be therapeutically targeted for cardioprotection.
In this Special Issue “Cardiac Fibrosis: From Pathogenesis to Targeted Therapies”, we are interested in the following topics:
- Novel mechanisms of heart diseases related to cardiac fibrosis, including myocardial infarction, ischemia/reperfusion injury, myocardial hypertrophy, myocarditis, cardiomyopathies and heart failure, etc.
- In vitro and/or in vivo studies of cardiac fibroblast activation and differentiation, as well as extracellular matrix protein production, secretion, and degradation.
- Novel therapeutics and techniques for the prevention and treatment of cardiac fibrosis.
- Novel biomarkers/imaging techniques for the detection and diagnosis of cardiac fibrosis.
Dr. Zhaokang Cheng
Dr. Xing Fu
Manuscript Submission Information
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- heart failure
- cardiac fibroblasts
- cardiac myocytes