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Published on: June 15, 2018
Circulating miR-10b-5p, miR-193a-3p, and miR-1-3p Are Deregulated in Patients with Heart Failure and Correlate with
Anna Maria Grimaldi1, Roberta D'Assante2, Francesco Fiore2
1IRCCS SYNLAB SDN, Via Emanuele Gianturco 113, 80143 Naples, Italy.
Insights
Circulating microRNAs (miRNAs) like miR-10b-5p, miR-193a-5p, and miR-1-3p can detect heart failure (HF) patients, especially those with multiple hormonal deficiencies (MHDS). These miRNAs are downregulated in HF and correlate with hormonal status, aiding in HF diagnosis.
Area of Science:
- Endocrinology
- Cardiology
- Molecular Biology
Background:
- Heart failure (HF) is a major global health burden.
- Anabolic hormonal axis reduction is implicated in HF progression.
- MicroRNAs (miRNAs) play roles in endocrine function and HF detection.
Purpose of the Study:
- To explore the association between circulating miRNA profiles and multiple hormonal deficiencies in HF patients.
- To provide new insights into HF pathophysiology.
- To assess the diagnostic potential of miRNAs in HF with hormonal deficiencies.
Main Methods:
- Plasma samples from 129 subjects (94 HF patients, 35 controls) were analyzed.
- Circulating miRNAs (miR-1-3p, miR-10b-5p, miR-24-3p, miR-193a-5p, miR-454-3p, miR-503-5p, miR-551b-3p, miR-598-3p) were measured.
- Hormone levels (IGF-1, fT3, DHEA-S, testosterone), NT-proBNP, HF subtypes, and NYHA class were evaluated. Multiple hormonal deficiency syndrome (MHDS) defined as ≥2 deficiencies.
Main Results:
- miR-10b-5p, miR-193a-5p, and miR-1-3p distinguished HF patients from controls.
- These miRNAs were downregulated in HF patients, particularly those with NYHA I-II and elevated NT-proBNP.
- The three miRNAs correlated with each other and were influenced by hormone deficiencies, especially in reduced ejection fraction patients.
- miR-10b-5p showed the highest diagnostic accuracy for chronic HF-MHDS patients (AUC = 0.8).
Conclusions:
- Circulating miR-10b-5p, miR-193a-5p, and miR-1-3p are potential biomarkers for detecting HF.
- These miRNAs are particularly useful in identifying HF patients with co-existing hormonal deficiencies.
- The findings support the clinical utility of these miRNAs in understanding HF pathophysiology and diagnosis.
Abstract:
Heart failure (HF) is among the most important causes of worldwide morbidity, hospitalisation, and mortality. A reduction in anabolic hormonal axes seems to potentially play an important role in chronic HF progression and prognosis. Several lines of evidence support the critical roles of miRNAs in the endocrine system, and differentially expressed miRNA patterns were found to be able to detect HF. To date, the ability of miRNAs to detect HF patients affected by hormonal deficiencies has yet to be addressed. The aim of this study was to explore the association between circulating miRNA profiles and multiple hormonal deficiencies in HF patients to provide new insights into HF pathophysiology. The study cohort included 129 subjects (94 HF patients and 35 controls). Circulating miRNAs assayed in plasma samples were miR-1-3p, miR-10b-5p, miR-24-3p, miR-193a-5p, miR-454-3p, miR-503-5p, miR-551b-3p, and miR-598-3p. NT-proBNP, IGF-1, fT3, DHEA-S, testosterone, HF subtypes, and NYHA class were also evaluated. A multiple hormonal deficiency syndrome (MHDS) was defined as the presence of ≥two hormone deficiencies. We found that miR-10b-5p, miR-193a-5p, and miR-1-3p could distinguish chronic HF patients from controls. The identified miRNAs were downregulated in HF patients, particularly those with NYHA I-II classifications and pathological values of NT-proBNP. In addition, these three circulating miRNAs correlated with each other, and their deregulation seems to be influenced by hormone deficiencies, especially in patients with reduced ejection fraction. Among the three miRNAs, miR-10b-5p was the best able to diagnose chronic HF-MHDS patients (AUC = 0.8). These results support the clinical utility of miR-10b-5p, miR-193a-5p, and miR-1-3p in detecting HF patients, especially those with hormone deficiencies.
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