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The Function and Therapeutic Potential of lncRNAs in Cardiac Fibrosis
Xiang Nie1,2, Jiahui Fan1,2, Dao Wen Wang1,2
1Division of Cardiology, Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
Insights
Long noncoding RNAs (lncRNAs) regulate cardiac fibrosis, a key factor in heart disease outcomes. Understanding lncRNA functions, especially exosome-derived ones, offers new therapeutic strategies for heart conditions.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Gene Regulation
Background:
- Cardiac fibrosis is a significant issue in cardiovascular diseases, impacting patient outcomes.
- Myocardial fibrosis progression can lead to ventricular remodeling and heart dysfunction.
- Complex molecular mechanisms, including TGF-β signaling and non-coding RNAs, regulate fibrosis.
Purpose of the Study:
- To summarize the role of long noncoding RNAs (lncRNAs) in cardiac fibrosis.
- To explore lncRNA involvement in miRNA expression, TGF-β signaling, and extracellular matrix synthesis.
- To highlight exosome-derived lncRNAs in regulating adverse fibrosis and their mechanisms.
Main Methods:
- Literature review and synthesis of recent studies on lncRNAs and cardiac fibrosis.
- Analysis of molecular pathways regulated by lncRNAs in myocardial fibrosis.
- Focus on exosomal lncRNAs and their secretion mechanisms.
Main Results:
- lncRNAs are critical regulators of gene expression in myocardial fibrosis.
- lncRNAs influence key fibrotic pathways, including TGF-β signaling and extracellular matrix dynamics.
- Exosome-mediated lncRNA transfer plays a role in regulating adverse cardiac fibrosis.
Conclusions:
- lncRNAs are pivotal in the development and progression of cardiac fibrosis.
- Exosome-derived lncRNAs represent a significant mechanism in fibrosis regulation.
- Targeting lncRNAs offers potential for novel therapeutic strategies against cardiac fibrosis.
Abstract:
Cardiac fibrosis remains an unresolved problem in cardiovascular diseases. Fibrosis of the myocardium plays a key role in the clinical outcomes of patients with heart injuries. Moderate fibrosis is favorable for cardiac structure maintaining and contractile force transmission, whereas adverse fibrosis generally progresses to ventricular remodeling and cardiac systolic or diastolic dysfunction. The molecular mechanisms involved in these processes are multifactorial and complex. Several molecular mechanisms, such as TGF-β signaling pathway, extracellular matrix (ECM) synthesis and degradation, and non-coding RNAs, positively or negatively regulate myocardial fibrosis. Long noncoding RNAs (lncRNAs) have emerged as significant mediators in gene regulation in cardiovascular diseases. Recent studies have demonstrated that lncRNAs are crucial in genetic programming and gene expression during myocardial fibrosis. We summarize the function of lncRNAs in cardiac fibrosis and their contributions to miRNA expression, TGF-β signaling, and ECMs synthesis, with a particular attention on the exosome-derived lncRNAs in the regulation of adverse fibrosis as well as the mode of action of lncRNAs secreted into exosomes. We also discuss how the current knowledge on lncRNAs can be applied to develop novel therapeutic strategies to prevent or reverse cardiac fibrosis.
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