Novel molecular plasma signatures on cardiovascular disease can stratify patients throughout life.

Cardiovascular risk stratification Organ damage markers Proteomic profile Risk prediction

Journal

Journal of proteomics
ISSN: 1876-7737
Titre abrégé: J Proteomics
Pays: Netherlands
ID NLM: 101475056

Informations de publication

Date de publication:
30 06 2020
Historique:
received: 14 01 2020
revised: 30 03 2020
accepted: 06 05 2020
pubmed: 12 5 2020
medline: 22 6 2021
entrez: 12 5 2020
Statut: ppublish

Résumé

Several models are available to calculate the risk of developing cardiovascular complications in mid-life. The estimation of lifetime risk in the long-term remains an unmet clinical need. We previously identified new molecular plasma signatures for cardiovascular risk stratification in a young population (30-50-years old). The aim of the present study was to determine if the specific signature found in young population changes with age. Proteomic analysis was performed in plasma samples obtained from different age groups, middle-age (50-70-years old, n = 63) and elderly (>70-years old, n = 61), which, in turn were classified into 3 subgroups according to cardiovascular risk. Our previous results in a young population clearly showed two different proteomic signatures. Building on these findings, targeted-mass spectrometry and turbidimetry analyses were used to test these signatures in middle-age and elderly populations. This strategy identified three common proteomic signatures between young and adult patients related to cardiovascular stratification, organ damage and risk prediction. Furthermore, receiver operating characteristic analysis revealed the potential value of these novel markers for lifetime risk stratification. Our results provide new insight into altered molecular mechanisms in the pathogenesis of cardiovascular disease and, more importantly, identify novel protein panels that can stratify patients throughout life. SIGNIFICANCE: Our results revealed three common proteomic signatures between young and adult patients related to cardiovascular stratification, organ damage and risk prediction. The results obtained provide a deeper insight into the pathogenesis of CV diseases and allow the identification of novel protein panels to stratify patients according to CV risk throughout life. While current estimators calculate the risk of having a CV event considering age as the most important factor to CV disease, our results represent an alternative to traditional CV risk factors, allowing the stratification of CV risk regardless of the age. Using a combination of traditional markers and established algorithms with these findings as a future preventive strategy, could facilitate an adequate assessment of CV risk.

Identifiants

pubmed: 32389841
pii: S1874-3919(20)30184-6
doi: 10.1016/j.jprot.2020.103816
pii:
doi:

Substances chimiques

Biomarkers 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

103816

Informations de copyright

Copyright © 2020 Elsevier B.V. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of competing interest The authors declare that they have no conflicts of interest.

Auteurs

Nerea Corbacho-Alonso (N)

Department of Vascular Physiopathology, Hospital Nacional de Parapléjicos, SESCAM, Toledo, Spain.

Montserrat Baldán-Martín (M)

Department of Vascular Physiopathology, Hospital Nacional de Parapléjicos, SESCAM, Toledo, Spain.

Juan Antonio López (JA)

Cardiovascular Proteomics Laboratory and CIBER-CV, CNIC, Madrid, Spain.

Elena Rodríguez-Sánchez (E)

Cardiorenal Translational Laboratory, Instituto de Investigación i+12, Hospital Universitario 12 de Octubre, Madrid, Spain.

Paula J Martínez (PJ)

Departament of Immunology, IIS-Fundacion Jimenez Diaz-UAM, Madrid, Spain.

Laura Mourino-Alvarez (L)

Department of Vascular Physiopathology, Hospital Nacional de Parapléjicos, SESCAM, Toledo, Spain.

Tatiana Martin-Rojas (T)

Department of Vascular Physiopathology, Hospital Nacional de Parapléjicos, SESCAM, Toledo, Spain.

Tamara Sastre-Oliva (T)

Department of Vascular Physiopathology, Hospital Nacional de Parapléjicos, SESCAM, Toledo, Spain.

Felipe Madruga (F)

Departament of Geriatrics, Hospital Virgen del Valle, SESCAM, Toledo, Spain.

Jesús Vázquez (J)

Cardiovascular Proteomics Laboratory and CIBER-CV, CNIC, Madrid, Spain.

Luis R Padial (LR)

Department of Cardiology, Hospital Virgen de la Salud, SESCAM, Toledo, Spain.

Gloria Alvarez-Llamas (G)

Departament of Immunology, IIS-Fundacion Jimenez Diaz-UAM, Madrid, Spain.

Fernando Vivanco (F)

Departament of Immunology, IIS-Fundacion Jimenez Diaz-UAM, Madrid, Spain.

Gema Ruiz-Hurtado (G)

Cardiorenal Translational Laboratory, Instituto de Investigación i+12, Hospital Universitario 12 de Octubre, Madrid, Spain.

Luis M Ruilope (LM)

Cardiorenal Translational Laboratory, Instituto de Investigación i+12, Hospital Universitario 12 de Octubre, Madrid, Spain; CIBER-CV, Hospital Universitario 12 de Octubre, Madrid, Spain; School of Doctoral Studies and Research, Universidad Europea de Madrid, Spain.

Maria G Barderas (MG)

Department of Vascular Physiopathology, Hospital Nacional de Parapléjicos, SESCAM, Toledo, Spain. Electronic address: megonzalezb@sescam.jccm.es.

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Classifications MeSH