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Overexpression of miR-221 in sudden death with cardiac hypertrophy patients
Yu Kakimoto1, Masayuki Tanaka2, Hideki Hayashi2
1Department of Forensic Medicine, Tokai University School of Medicine, Kanagawa, Japan.
Insights
Sudden cardiac death (SCD) in cardiac hypertrophy is hard to predict. This study found elevated miR-221 levels in SCD with cardiac hypertrophy (SCH) patients, suggesting it may indicate a higher risk for lethal outcomes.
Area of Science:
- Cardiovascular Research
- Molecular Biology
- Genetics
Background:
- Cardiac hypertrophy is a risk factor for heart failure and sudden cardiac death (SCD).
- Predicting SCD in asymptomatic cardiac hypertrophy is challenging.
- MicroRNAs (miRNAs) are key regulators in heart failure progression.
Purpose of the Study:
- To investigate alterations in miRNA expression in sudden cardiac death with cardiac hypertrophy (SCH).
- To identify potential miRNA biomarkers for SCD risk in cardiac hypertrophy.
Main Methods:
- Autopsy-obtained cardiac tissues from SCH, compensated cardiac hypertrophy (CCH), and control groups.
- Histopathological examination of cardiac tissues.
- Deep sequencing and quantitative PCR for cardiac miRNA analysis.
Main Results:
- Distinct miRNA expression signatures were observed between SCH and CCH, despite similar histology.
- Eight miRNAs were differentially expressed between SCH and CCH.
- miR-221 was significantly elevated in SCH compared to CCH and control cases.
Conclusions:
- Elevated cardiac miR-221 levels in SCH patients correlate with lethal outcomes.
- Increased miR-221 may be a potential biomarker for increased SCD risk in cardiac hypertrophy.
- miRNA profiling offers insights into the mechanisms underlying SCD in cardiac hypertrophy.
Background:
Cardiac hypertrophy is a well-known risk factor for heart failure and sudden cardiac death (SCD). On the other hand, physiological cardiac hypertrophy is often observed in young healthy men, and it is difficult to predict SCD in cardiac hypertrophy subjects who do not show symptoms of heart failure. MicroRNAs (miRNAs) widely regulate biological activity and play pivotal roles in heart failure progression. In this study, we investigated whether miRNA expression is altered in SCD with cardiac hypertrophy (SCH).
Methods:
Cardiac tissues were sampled at autopsy from SCH patients, compensated cardiac hypertrophy (CCH) subjects who died of causes other than heart failure, and control cases without cardiac hypertrophy or heart failure. After histopathological examination, we performed deep sequencing and quantitative PCR of cardiac miRNAs.
Results And Discussion:
Although SCH and CCH showed indistinguishable histological features, their miRNA expression signatures were distinct. Among the 240 miRNAs stably detected in the heart, 8 were differentially expressed between SCH and CCH. Specifically, miR-221 increased in SCH compared to CCH and control cases. The significant elevation of cardiac miR-221 in SCH patients is correlated with lethal outcomes. Thus, our results indicate that an elevated miR-221 level is potentially associated with an increased risk of SCD in subjects with cardiac hypertrophy.
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