Evidence map›Paper›PMID 40277943›Full record

ReviewCells2025

Mitochondrial Dysfunction: A New Hallmark in Hereditable Thoracic Aortic Aneurysm Development.

Daniel Marcos-Ríos, Antonio Rochano-Ortiz, Irene San Sebastián-Jaraba, María José Fernández-Gómez, Nerea Méndez-Barbero, Jorge Oller

Abstract readReview
In one paragraph

Review in Cells, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
–field-weighted citation impact
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

16 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
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  6. Pain Hypersensitivity in a Mouse Model of Marfan Syndrome.Antioxidants (Basel, Switzerland) · 2026
    Article
  7. Review
  8. Article
  9. Article
  10. Journal of inflammation research · 2026
    Article
  11. Article
  12. Article
  13. Review
  14. Article
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  16. 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

6 authors.

Daniel Marcos-RíosLaboratory of Vascular Pathology, Health Research Institute-Fundación Jiménez Díaz University Hospital, Universidad Autónoma de Madrid (IIS-FJD, UAM), 28040 Madrid, Spain.ORCID 0009-0006-2872-1573
Antonio Rochano-OrtizLaboratory of Vascular Pathology, Health Research Institute-Fundación Jiménez Díaz University Hospital, Universidad Autónoma de Madrid (IIS-FJD, UAM), 28040 Madrid, Spain.ORCID 0009-0006-1456-2946
Irene San Sebastián-JarabaLaboratory of Vascular Pathology, Health Research Institute-Fundación Jiménez Díaz University Hospital, Universidad Autónoma de Madrid (IIS-FJD, UAM), 28040 Madrid, Spain.
María José Fernández-GómezLaboratory of Vascular Pathology, Health Research Institute-Fundación Jiménez Díaz University Hospital, Universidad Autónoma de Madrid (IIS-FJD, UAM), 28040 Madrid, Spain.
Nerea Méndez-BarberoLaboratory of Vascular Pathology, Health Research Institute-Fundación Jiménez Díaz University Hospital, Universidad Autónoma de Madrid (IIS-FJD, UAM), 28040 Madrid, Spain.
Jorge OllerLaboratory of Vascular Pathology, Health Research Institute-Fundación Jiménez Díaz University Hospital, Universidad Autónoma de Madrid (IIS-FJD, UAM), 28040 Madrid, Spain.ORCID 0000-0002-2224-2954

Funding

Instituto de Salud Carlos III PI24/00180Ministerio de Ciencia e Innovación PID2022-1377300A-100
6 · The paper itself

Abstract

Thoracic aortic aneurysms (TAAs) pose a significant health burden due to their asymptomatic progression, often culminating in life-threatening aortic rupture, and due to the lack of effective pharmacological treatments. Risk factors include elevated hemodynamic stress on the ascending aorta, frequently associated with hypertension and hereditary genetic mutations. Among the hereditary causes, Marfan syndrome is the most prevalent, characterized as a connective tissue disorder driven by

Indexed as

Aortic Aneurysm, ThoracicMitochondriaAnimalsHumansLoeys-Dietz SyndromeMarfan SyndromeMutationaneurysmconnective tissueMarfanmitochondriasmooth muscle cellsvascular pathology

Identifiers

PMID40277943
PMCPMC12026022

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.