Evidence map›Paper›PMID 32729659›Full record

ArticleAging cell2020

Identification of common cardiometabolic alterations and deregulated pathways in mouse and pig models of aging.

Víctor Fanjul, Inmaculada Jorge, Emilio Camafeita, Álvaro Macías, Cristina González-Gómez, Ana Barettino, Beatriz Dorado, María Jesús Andrés-Manzano, José Rivera-Torres, Jesús Vázquez and 2 more

Open access · goldAbstract read
In one paragraph

Article in Aging cell, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.3field-weighted citation impact, top 20% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. Cellular and molecular mechanisms underlying cardiovascular aging.Cellular & molecular biology letters · 2025
    Review
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  13. Genomic instability in the naturally and prematurely aged myocardium.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  14. Review
  15. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 2 institutions in 1 country.

Víctor FanjulCentro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain.ORCID 0000-0003-4009-4219
Inmaculada JorgeCentro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain.ORCID 0000-0001-8645-9477
Emilio CamafeitaCentro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain.ORCID 0000-0002-4577-5331
Álvaro MacíasCentro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain.ORCID 0000-0002-9952-6947
Cristina González-GómezCentro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain.
Ana BarettinoCentro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain.ORCID 0000-0001-9278-8488
Beatriz DoradoCentro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain.ORCID 0000-0002-1958-4558
María Jesús Andrés-ManzanoCentro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain.
José Rivera-TorresCentro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain.ORCID 0000-0003-0365-9604
Jesús VázquezCentro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain.ORCID 0000-0003-1461-5092
Carlos López-OtínDepartamento de Bioquímica y Biología Molecular, Facultad de Medicina, Instituto Universitario de Oncología, Universidad de Oviedo, Oviedo, Spain.ORCID 0000-0001-6964-1904
Vicente AndrésCentro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain.ORCID 0000-0002-0125-7209
Spanish National Centre for Cardiovascular Research · ESUniversidad de Oviedo · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aging is the main risk factor for cardiovascular and metabolic diseases, which have become a global concern as the world population ages. These diseases and the aging process are exacerbated in Hutchinson-Gilford progeria syndrome (HGPS or progeria). Here, we evaluated the cardiometabolic disease in animal models of premature and normal aging with the aim of identifying alterations that are shared or specific to each condition. Despite differences in body composition and metabolic markers, prematurely and normally aging mice developed heart failure and similar cardiac electrical abnormalities. High-throughput proteomics of the hearts of progeric and normally aged mice revealed altered protein oxidation and glycation, as well as dysregulated pathways regulating energy metabolism, proteostasis, gene expression, and cardiac muscle contraction. These results were corroborated in the hearts of progeric pigs, underscoring the translational potential of our findings, which could help in the design of strategies to prevent or slow age-related cardiometabolic disease.

Indexed as

AgingAnimalsCardiovascular DiseasesDisease Models, AnimalHumansMiceProgeriaProteomicsSwineagingcardiometabolic diseaseHGPSHutchinson-Gilford progeria syndromemouse modelspathophysiologypig modelsproteomics

Identifiers

PMID32729659
PMCPMC7511870
OpenAlexW3045557308

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.