Progress on long non-coding RNAs in calcific aortic valve disease

Yan Shen1, Jiahui Li1, Zehao Zhao2

  • 1Department of Cardiology, The First Affiliated Hospital of Ningbo University, Ningbo, China.

PubMed

Insights

Long non-coding RNAs (lncRNAs) are key regulators in calcific aortic valve disease (CAVD). This review explores how lncRNAs like H19, MALAT1, and TUG1 influence CAVD progression and offers insights into potential therapeutic targets.

Area of Science:

  • Cardiovascular Biology
  • Molecular Genetics
  • RNA Biology

Background:

  • Calcific aortic valve disease (CAVD) is a prevalent condition in older adults, characterized by aortic valve fibrosis and calcification.
  • Pathological mechanisms include endothelial dysfunction, inflammation, oxidative stress, and lipid metabolism disorders, leading to stenosis.
  • Long non-coding RNAs (lncRNAs) are increasingly recognized as critical gene expression regulators in disease pathogenesis.

Purpose of the Study:

  • To review the mechanisms by which lncRNAs contribute to the development and progression of CAVD.
  • To identify specific lncRNAs, such as H19, MALAT1, and TUG1, implicated in CAVD.
  • To discuss the potential of lncRNAs as therapeutic targets for CAVD.

Main Methods:

  • Literature review of studies investigating lncRNAs in CAVD.
  • Analysis of lncRNA roles in regulating valve interstitial cell osteogenic differentiation and inflammation.
  • Examination of lncRNA-mediated gene expression modulation, including miRNA sponging and regulatory networks.

Main Results:

  • lncRNAs play a significant role in the pathological processes of CAVD.
  • Specific lncRNAs (H19, MALAT1, TUG1) are closely associated with CAVD.
  • lncRNAs can modulate calcification-related genes through complex regulatory mechanisms.

Conclusions:

  • lncRNAs are critical regulators in CAVD pathogenesis.
  • Targeting lncRNAs offers a promising therapeutic strategy for CAVD.
  • Further research into lncRNA function can uncover novel treatment approaches for this condition.