miR-222 inhibits pathological cardiac hypertrophyand heart failure.
Xiaojun LiuHaobo LiMargaret H HastingsChunyang XiaoFederico DamilanoColin PlattCarolin LerchenmüllerHan ZhuXin Paul WeiAshish YeriPatrick MostAnthony RosenzweigPublished in: Cardiovascular research (2023)
We report that miR-222 was necessary and sufficient to limit cardiac growth, cardiomyocyte cell death, adverse ventricular remodeling, and cardiac dysfunction in response to pressure overload. This suggests possible therapeutic value, particularly as miR-222 is conserved between mice and humans and regulated by exercise in both.
Keyphrases
- left ventricular
- cell proliferation
- heart failure
- long non coding rna
- cell death
- long noncoding rna
- oxidative stress
- physical activity
- transcription factor
- cardiac resynchronization therapy
- metabolic syndrome
- angiotensin ii
- resistance training
- body composition
- adipose tissue
- insulin resistance
- signaling pathway
- endothelial cells
- catheter ablation