Dataset related to the article: "Impact of Sacubitril/Valsartan on Circulating microRNA in Patients with Heart Failure"
Authors/Creators
- 1. Centro Cardiologico Monzino IRCCS
- 2. Cardiovascular Section, Department of Clinical Sciences and Community Health, University of Milan; Centro Cardiologico Monzino IRCCS
- 3. Università di Pavia, Dipartimento di Biologia e Biotecnologie "Lazzara Spallanzani"; Centro Cardiologico Monzino IRCCS
Description
This record contains raw data related to the article "Impact of Sacubitril/Valsartan on Circulating microRNA in Patients with Heart Failure"
Abstract: Sacubitril/Valsartan, used for the treatment of heart failure (HF), is a combination of two drugs, an angiotensin receptor inhibitor, and a neprilysin inhibitor, which activates vasoactive peptides. Even though its beneficial effects on cardiac functions have been demonstrated, the mechanisms underpinning these effects remain poorly understood. To achieve more mechanistic insights, we analyzed the profiles of circulating miRNAs in plasma from patients with stable HF with reduced ejection function (HFrEF) and treated with Sacubitril/Valsartan for six months. miRNAs are short (22–24 nt) non-coding RNAs, which are not only emerging as sensitive and stable biomarkers for various diseases but also participate in the regulation of several biological processes. We found that in patients with high levels of miRNAs, specifically miR-29b-3p, miR-221-3p, and miR-503-5p, Sacubitril/Valsartan significantly reduced their levels at follow-up. We also found a significant negative correlation of miR-29b-3p, miR-221-3p, and miR-503-5p with VO2 at peak exercise, whose levels decrease with HF severity. Furthermore, from a functional point of view, miR-29b-3p, miR-221-3p, and miR-503-5p all target Phosphoinositide-3-Kinase Regulatory Subunit 1, which encodes regulatory subunit 1 of phosphoinositide-3-kinase. Our findings support that an additional mechanism through which Sacubitril/Valsartan exerts its functions is the modulation of miRNAs with potentially relevant roles in HFrEF pathophysiology.
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- Is supplement to
- 10.3390/biomedicines11041037 (DOI)
Funding
- Ministry of Health
- Ricerca Corrente to Centro Cardiologico Monzino IRCCS RC