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Updated: May 13, 2026

Magnetic Adjustment of Afterload in Engineered Heart Tissues
Published on: May 5, 2020
Choline protects against cardiac hypertrophy induced by increased after-load
Yilei Zhao1, Chen Wang, Jianwei Wu
1Institute of Clinical Pharmacology, the Second Affiliated Hospital of Harbin Medical University, China.
Choline supplementation shows cardioprotective effects against cardiac hypertrophy by restoring miR-133a and calcineurin levels. This suggests choline may be a valuable adjunct therapy for preventing heart enlargement.
Area of Science:
- Cardiovascular Research
- Nutritional Science
- Molecular Cardiology
Background:
- Inadequate choline intake is linked to increased cardiovascular risk.
- The protective role of choline supplementation against cardiac hypertrophy remains unstudied.
Purpose of the Study:
- To investigate the effects of choline supplementation on cardiac hypertrophy.
- To explore the underlying molecular mechanisms of choline's cardioprotective action.
Main Methods:
- Cardiac hypertrophy was induced in mice via transverse aorta constriction (TAC) and in cultured cardiomyocytes using isoproterenol (ISO).
- Choline's effects were assessed using Western blot and real-time PCR to analyze key hypertrophy markers (ANP, BNP, β-MHC) and signaling molecules (miR-133a, Calcineurin).
- The role of muscarinic acetylcholine receptors (mAChR) was investigated using a specific antagonist.
Main Results:
- Choline supplementation significantly attenuated cardiac hypertrophy in mice and cultured cells, reducing heart weight and ventricular thickness.
- Choline administration normalized the expression of cardiac hypertrophy biomarkers.
- Choline restored the expression of the anti-hypertrophic microRNA miR-133a and reduced elevated calcineurin levels, effects blocked by a mAChR antagonist.
Conclusions:
- Choline demonstrates significant cardioprotection against cardiac hypertrophy.
- The mechanism involves the modulation of miR-133a and calcineurin pathways.
- Choline supplementation may serve as an effective adjunct therapy for preventing and treating cardiac hypertrophy.
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