Key result
Carvedilol in HFrEF is linked to ~5-fold higher circulating miR-1 and miR-214 levels.
Why the study?
Although carvedilol produces cytoprotective actions against cardiomyocyte hypertrophy in heart failure, the underlying mechanisms remain poorly understood.
Does carvedilol alter the expression of hypertrophic-specific miRNAs in patients with systolic heart failure?
Observational (n=72)
Does carvedilol alter the expression of hypertrophic-specific miRNAs in patients with systolic heart failure?
Carvedilol therapy in systolic heart failure is associated with upregulation of circulating miR-1 and miR-214, suggesting a potential epigenetic mechanism for its cardioprotective effects.
Carvedilol was associated with miR-1/miR-214 upregulation in systolic HF; hypothesis-generating for epigenetic effects and requires prospective validation.
Introduction: MicroRNAs (miRNAs) are recognized as major contributors in various cardiovascular diseases, such as heart failure (HF). These small noncoding RNAs that posttranscriptionally control target genes are involved in regulating different pathophysiological processes including cardiac proliferation, ifferentiation, hypertrophy, and fibrosis. Although carvedilol, a β-adrenergic blocker, and a drug of choice in HF produce cytoprotective actions against cardiomyocyte hypertrophy, the mechanisms are poorly understood. Here we proposed that the expression of hypertrophic-specific miRNAs (miR-1, miR-133, miR-208, and miR-214) might be linked to beneficial effects of carvedilol. Methods: The levels of four hypertrophic-specific miRNAs were measured in the sera of 35 patients with systolic HF receiving carvedilol (treated) and 20 HF patients not receiving any β-blockers (untreated) as well as 17 nonHF individuals (healthy) using quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Systolic HF was defined as left ventricular ejection fraction < 50% by transthoracic echocardiography. Results: We demonstrated that miR-1 and miR-214 were significantly upregulated in the treated group compared to the untreated group ( P =0.014 and 5.3-fold, 0.033 and 4.2-fold, respectively). However, miR-133 and miR-208 did not show significant difference in expression between these two study groups. MiR-1 was significantly downregulated in the untreated group compared with healthy individuals ( P =0.019 and 0.14-fold). Conclusion: In conclusion, it might be postulated that one of the mechanisms by which carvedilol may exert its cardioprotective effects can be through increasing miR-1 and miR-214 expressions which may also serve as a potential therapeutic target in patients with systolic HF in future.
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Shirazi-Tehrani et al. (2020) conducted an observational in Systolic heart failure (n=72). Carvedilol vs. No β-blockers (untreated) and healthy individuals was evaluated on Levels of four hypertrophic-specific miRNAs (miR-1, miR-133, miR-208, and miR-214) (Fold change 5.3 (miR-1) and 4.2 (miR-214), p=0.014 (miR-1), 0.033 (miR-214)). Carvedilol treatment in systolic heart failure was associated with significant upregulation of circulating miR-1 (5.3-fold, P=0.014) and miR-214 (4.2-fold, P=0.033) compared to untreated patients.
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