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Long Non-Coding RNAs in Cardiac Remodeling
Shutong Shen1, Huimin Jiang2,3, Yihua Bei4,5
1Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Insights
Long non-coding RNAs (lncRNAs) significantly modify cardiac remodeling, impacting heart disease progression. Targeting lncRNA expression offers promising therapeutic strategies for cardiovascular diseases.
Area of Science:
- Cardiovascular Biology
- Molecular Genetics
- Epigenetics
Background:
- Cardiac remodeling, a pathological process involving cardiomyocyte hypertrophy, apoptosis, and extracellular matrix changes, underlies cardiovascular disease progression.
- Long non-coding RNAs (lncRNAs) are increasingly recognized as critical regulators of cardiac remodeling.
- Specific lncRNAs have been linked to various aspects of cardiac remodeling, including hypertrophy, cell loss, and vascular dysfunction.
Purpose of the Study:
- To review the role of lncRNAs in cardiac remodeling.
- To highlight specific lncRNAs involved in different pathological processes of cardiac remodeling.
- To explore the therapeutic potential of modulating lncRNA expression in cardiovascular diseases.
Main Methods:
- Literature review of studies investigating lncRNAs in cardiac remodeling.
- Analysis of implicated lncRNAs in cardiac hypertrophy, cardiomyocyte loss, extracellular matrix remodeling, and vascular cell dysfunction.
- Synthesis of findings regarding the regulatory functions of lncRNAs in the heart.
Main Results:
- Numerous lncRNAs (e.g., Chaer, Chast, Mhrt, CHRF, ROR, H19, MIAT, NRF, APF, CARL, UCA) are implicated in cardiac hypertrophy and cardiomyocyte loss.
- Specific lncRNAs (MALAT1, TGFB2-OT1, lincRNA-p21, lnc-Ang362) are involved in vascular endothelial and smooth muscle cell dysfunction and proliferation.
- lncRNAs act as dynamic modifiers of the pathological processes in cardiac remodeling.
Conclusions:
- lncRNAs play a crucial role in regulating cardiac remodeling and cardiovascular disease progression.
- Modulating lncRNA expression, by inhibiting disease-up-regulated or increasing disease-down-regulated lncRNAs, presents a novel therapeutic avenue.
- Targeting lncRNAs offers a promising strategy for treating cardiac remodeling and related cardiovascular diseases.
Abstract:
Cardiac remodeling occurs after stress to the heart, manifested as pathological processes, including hypertrophy and apoptosis of cardiomyocytes, dysfunction of vascular endothelial cells and vascular smooth muscle cells as well as differentiation and proliferation of fibroblasts, ultimately resulting in progression of cardiovascular diseases. Emerging evidence has revealed that long non-coding RNAs (lncRNAs) acted as powerful and dynamic modifiers of cardiac remodeling. LncRNAs including Chaer, Chast, Mhrt, CHRF, ROR, H19, and MIAT have been implicated in cardiac hypertrophy while NRF, H19, APF, CARL, UCA, Mhrt and several other lncRNAs (n379599, n379519, n384640, n380433 and n410105) in cardiomyocyte loss and extracellular matrix remodeling. In addition, MALAT1 and TGFB2-OT1 have been reported to contribute to vascular endothelial cells dysfunction while lincRNA-p21 and lnc-Ang362 to vascular smooth muscle cells proliferation. Thus, manipulation of lncRNA expression levels through either the inhibition of disease-up-regulated lncRNAs or increasing disease-down-regulated lncRNAs represents novel therapeutic strategies for cardiac remodeling.