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lncRNA - Long Non-coding RNAs02:39

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Related Experiment Video

Updated: Mar 22, 2026

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes
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Long Non-Coding RNA-ROR Mediates the Reprogramming in Cardiac Hypertrophy.

Feng Jiang1, Xiangyu Zhou2, Jing Huang1

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Long non-coding RNA-ROR (lncRNA-ROR) promotes cardiac hypertrophy by interacting with miR-133. Downregulating lncRNA-ROR may offer a therapeutic strategy for treating cardiac hypertrophy.

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Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Epigenetics

Background:

  • Cardiac hypertrophy is a major risk factor for heart failure and sudden death.
  • Understanding hypertrophy mechanisms is crucial for developing new therapies.
  • The role of long non-coding RNAs (lncRNAs) in cardiomyocyte reprogramming is largely unknown.

Purpose of the Study:

  • To investigate the functional role of lncRNA-ROR in cardiac hypertrophy.
  • To elucidate the molecular mechanisms underlying lncRNA-ROR's function in the heart.

Main Methods:

  • Quantitative real-time PCR to measure gene expression.
  • In vitro studies using cardiomyocytes treated with phenylephrine.
  • Knockdown and overexpression of lncRNA-ROR and miR-133.

Main Results:

  • lncRNA-ROR expression is significantly upregulated in cardiac hypertrophy.
  • Downregulation of lncRNA-ROR attenuates hypertrophic responses in cardiomyocytes.
  • lncRNA-ROR negatively regulates miR-133 expression, and miR-133 overexpression counteracts hypertrophy-induced gene expression.

Conclusions:

  • lncRNA-ROR promotes cardiac hypertrophy through interaction with miR-133.
  • lncRNA-ROR represents a potential therapeutic target for antihypertrophic treatments.