The miR-21 expression is more valuable than the miR-1 expression in predicting cardiovascular events of acute HF and the combined analysis of miR-21 expression, galectin-3, and NT-proBNP can increase the predictive value of miR-21 expression.
Both iptakalim and natakalim significantly upregulated the expression of miR-1-3p, suggesting that this miR is closely associated with the therapeutic effects against chronic heart failure.
It has been shown that miR-1 can reverse cardiac hypertrophy during the compensatory phase of HF development, but it is unknown whether miR-1 can still reverse cardiac dysfunction and improve cardiac remodeling after HF progresses to the decompensation stage.
The decreased expression of muscle-specific microRNA-1 (miR-1) has been found in many cardiovascular diseases and is considered to contribute to heart failure (HF).
Based on previous findings, the expression of 13 different microRNAs involving heart failure and hypertrophy (miR-1-3p, miR-10b, miR-21, miR-23a, miR-27a, miR-29a, miR-133a-3p, miR-142-3p, miR-155, miR-199a-3p, miR-199a-5p, miR-214, miR-497) was measured.
Myocardial biopsy specimens taken from Chinese patients presenting with recent heart failure were compared with a group of patients without heart failure undergoing routine cardiac surgery (n=34). miRNAs (miR-1, -21, -23, -29, -30, -130, -133, -195, -199, -208, and -320) and corresponding mRNA expression were measured by real-time quantitative-PCR method. miR-1, -21, -23, -29, -130, -195 and -199 were significantly up-regulated in the heart failure group when compared to those without heart failure (all p<0.01).
MicroRNAs (miRNAs) play a key role in the development of heart failure, and recent studies have shown that the muscle-specific miR-1 is a key regulator of cardiac hypertrophy.
Cardio-enriched miRNAs (miR-1, miR-208b and miR-499-5p) were measured using real time PCR in plasma samples from 424 patients with suspected ACS treated in a coronary care unit. miRNAs were assessed for discrimination of a clinical diagnosis of myocardial infarction and for association with 30-day mortality and diagnosis of heart failure.
These findings demonstrate the importance of miR-1 in cardiac function and in the pathogenesis of heart failure via Sorcin-dependent calcium homeostasis.
We studied hearts isolated from canines with chronic HF exhibiting increased left ventricular (LV) dimensions and decreased LV contractility. qRT-PCR revealed that the levels of miR-1 and miR-133, the most abundant muscle-specific miRNAs, were significantly increased in HF myocytes compared with controls (2- and 1.6-fold, respectively).