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A circulating MicroRNA signature for the diagnosis of pulmonary arterial hypertension and functional characterization of candidate miR-3168
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  • Published: 05 March 2026

A circulating MicroRNA signature for the diagnosis of pulmonary arterial hypertension and functional characterization of candidate miR-3168

  • Mauro Lago-Docampo1,2 nAff7,
  • Ainhoa Iglesias-López1,
  • Carlos Vilariño3,
  • Adolfo Baloira4,
  • Joan Albert Barberá5,6,
  • Isabel Blanco5,6 &
  • …
  • Diana Valverde1,2,8 

Scientific Reports , Article number:  (2026) Cite this article

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Subjects

  • Biomarkers
  • Cardiology
  • Diseases
  • Genetics
  • Medical research
  • Molecular biology

Abstract

Pulmonary Arterial Hypertension (PAH) is a rare, progressive disorder characterized by pathological vascular remodeling of the pulmonary arteries, ultimately leading to right heart failure. Early diagnosis remains challenging, as clinical manifestations are often nonspecific, and definitive confirmation still requires invasive right heart catheterization. Circulating microRNAs (miRNAs) have emerged as promising biomarkers for cardiovascular diseases due to their plasma stability and direct involvement in disease pathophysiology. We performed small RNA sequencing on plasma samples from 25 IPAH patients and 10 healthy controls to identify differentially expressed miRNAs. Seven candidate miRNAs were selected for further validation by quantitative PCR in a multicenter cohort of 110 IPAH patients and controls. Logistic regression models were built to evaluate diagnostic performance. Functional studies for miR-3168 were performed using western blot and flow cytometry in Pulmonary Artery Endothelial Cells (PAECs), and tube formation assay in human umbilical vein endothelial cells (HUVECs). Our initial screen identified 29 differentially expressed miRNAs. Seven of these candidates, including members of the let-7 family and miR-3168, were successfully validated in the larger cohort. A diagnostic panel incorporating three miRNAs (let-7a-5p, miR-9-5p, and miR-31-5p) was developed, which achieved an area under the curve (AUC) of 0.862 (95% CI = 0.7481–1) for discriminating PAH patients from controls. Separately, we investigated the functional role of miR-3168, which was upregulated in PAH patients. In PAECs, overexpression of miR-3168 led to a reduction of BMPR2 protein levels. Moreover, miR-3168 overexpression impaired tube formation in HUVECs. Our study identifies a plasma-derived three-miRNA signature with strong potential for the non-invasive diagnosis of PAH. Furthermore, we implicate miR-3168 as a potential contributor to endothelial dysfunction through its regulation of BMPR2 and its anti-angiogenic effects in vitro. These findings reinforce the dual utility of circulating miRNAs as both clinically relevant non-invasive biomarkers and as tools to discover novel disease biology.

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Data availability

All data generated in this article is available upon request to the corresponding author. RNA-seq derived data is freely available at GSE222022, DESeq2 analysis table can be accessed in the supplementary dataset.

Abbreviations

3′UTR:

3′ Untranslated region

6MWD:

6-Minute walking distance

AUC:

Area under the curve

BMPR1A:

Bone morphogenetic protein receptor type 1A

BMPR2:

Bone morphogenetic protein receptor type 2

BNP:

Brain natriuretic peptide

DCs:

Dendritic cells

DE:

Differentially expressed

EDN1/ET-1:

Endothelin 1

FC-NYHA:

Functional class in the New York Heart Association

FDR:

False discovery rate

HDAC2:

Histone deacetylase 2

HPAH:

Heritable pulmonary arterial hypertension

HUVECs:

Human umbilical vein endothelial cells

iNO:

Inhaled nitric oxide

IPAH:

Idiopathic pulmonary arterial hypertension

miRNAs:

MicroRNAs

NT-proBNP:

N-terminal pro b-type natriuretic peptide

PAECs:

Pulmonary arterial endothelial cells

PAH:

Pulmonary arterial hypertension

PCA:

Principal component analysis

PVR:

Pulmonary vascular resistance

qPCR:

Quantitative polymerase chain reaction

RHC:

Right heart catheterization

RNA:

Ribonucleic acid

ROC:

Receiver operating characteristic

SMC:

Smooth Muscle Cell

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Acknowledgements

We thank all the patients that participated in this study and all the clinical personnel implied in sample retrieval and the IDIBAPS Biobank. We thank the REHAP investigators for their effort to recruit and manage the patients. We thank Fundación Contra la Hipertensión Pulmonar for their continues support and effort. We thank Laura Muinelo Romay for providing us with the controls for the discovery cohort. We thank Merce Peleteiro from the Cytometry core facility of CINBIO for her technical help. In loving memory of Guillermo Pousada.

Funding

This study was partially funded by grants from Fundación Contra la Hipertensión Pulmonar, Jansen Pharmaceuticals, Ministerio de Ciencia e Innovación (PI18/01233, PI24/01182, Xunta de Galicia Axudas para consolidación e estructuración de unidades de investigación competitivas e outras accións de fomento (GRC-ED431C 2022/26) to DV. MLD was supported by a Xunta de Galicia predoctoral fellowship (ED481A-2018/304). AIG was supported by a collaboration grant from Ministerio de Educación y Formación Profesional 2020–21. This research was funded by the AGAUR Catalan Agency, grant number 2021_SGR_01493.

Author information

Author notes

  1. Mauro Lago-Docampo

    Present address: Biochemistry and Molecular Biology, Facultad de Biología, Universidade de Vigo, Lagoas Marcosende s/n, 36310, Vigo, Spain

Authors and Affiliations

  1. CINBIO, Universidade de Vigo, Vigo, Spain

    Mauro Lago-Docampo, Ainhoa Iglesias-López & Diana Valverde

  2. Rare Diseases and Pediatric Medicine, Galicia Sur Health Research Institute (IIS Galicia Sur), SERGAS-UVIGO, Vigo, Spain

    Mauro Lago-Docampo & Diana Valverde

  3. Pneumology Department, Hospital Povisa, Vigo, Spain

    Carlos Vilariño

  4. Pneumology Department, Complejo Hospitalario Universitario de Pontevedra, SERGAS, Galicia, Spain

    Adolfo Baloira

  5. Department of Pulmonary Medicine, Hospital Clínic-Fundació de Recerca Clínic Barcelona-Institut d’Investigacions Biomèdiques August Pi i Sunyer (FRCB-IDIBAPS), University of Barcelona, Barcelona, Spain

    Joan Albert Barberá & Isabel Blanco

  6. Biomedical Research Networking Center on Respiratory Diseases (CIBERES), Madrid, Spain

    Joan Albert Barberá & Isabel Blanco

  7. Department of Pediatrics –Cardiology, Stanford University School of Medicine, Stanford, CA, USA

    Diana Valverde

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Contributions

MLD and DV designed and conceptualized the study. MLD performed all the experimental and analysis work. AIG assisted in the validation cohort analyses. MLD wrote the manuscript. AB, CV, JAB and IB collected samples and retrieved clinical history. DV supervised the study. All authors approved the manuscript.

Corresponding author

Correspondence to Diana Valverde.

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The authors declare no competing interests.

Ethical approval and consent to participate

The study was conducted with the approval of the Comité de ética da Investigación de Galicia (CEIC Galicia). Written informed consent was obtained from all patients and control participants included in this study.

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Lago-Docampo, M., Iglesias-López, A., Vilariño, C. et al. A circulating MicroRNA signature for the diagnosis of pulmonary arterial hypertension and functional characterization of candidate miR-3168. Sci Rep (2026). https://doi.org/10.1038/s41598-026-42550-8

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  • Received: 29 August 2025

  • Accepted: 26 February 2026

  • Published: 05 March 2026

  • DOI: https://doi.org/10.1038/s41598-026-42550-8

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Keywords

  • Pulmonary arterial hypertension
  • microRNA
  • Diagnosis
  • miR-3168
  • Angiogenesis
  • BMPR2
  • Biomarker
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