Evidence map›Paper›PMID 42193944›Full record

ReviewCells2026

Structural and Signaling Mechanisms of Aortic Wall Failure in Heritable Thoracic Aortic Disease.

Norifumi Takeda, Hiroki Yagi, Takayuki Fujiwara, Hitomi Aono-Setoguchi, Ryo Inuzuka, Issei Komuro

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Cells, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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.

Norifumi TakedaThe Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan.ORCID 0000-0003-4818-3347
Hiroki YagiMarfan Syndrome Center, The University of Tokyo Hospital, Tokyo 113-8655, Japan.ORCID 0000-0001-6615-6196
Takayuki FujiwaraDepartment of Cardiovascular Medicine, The University of Tokyo Hospital, Tokyo 113-8655, Japan.ORCID 0000-0002-8719-3997
Hitomi Aono-SetoguchiMarfan Syndrome Center, The University of Tokyo Hospital, Tokyo 113-8655, Japan.ORCID 0009-0009-5341-7241
Ryo InuzukaMarfan Syndrome Center, The University of Tokyo Hospital, Tokyo 113-8655, Japan.
Issei KomuroDepartment of Frontier Cardiovascular Science, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.

Funding

Fugaku Trust for Medical Research noneGout and Uric Acid Foundation of Japan noneJapan Agency for Medical Research and Development JP24ek0109755hJapan Agency for Medical Research and Development JP24ek0109766hJapan Agency for Medical Research and Development JP25tm0424702sJapan Foundation for Applied Enzymology noneJapan Heart Foundation noneOkinaka Memorial Institute for Medical Research noneThe Ichiro Kanehara Foundation none
6 · The paper itself

Abstract

Heritable thoracic aortic diseases (HTAD) are inherited conditions that increase the risk of thoracic aortic aneurysms, dissections, and premature aortic rupture. Advances in human genetics and experimental models have transformed our understanding of these disorders from a phenotype-based classification system to a mechanism-based view involving extracellular matrix (ECM) architecture, transforming growth factor-β (TGFβ) signaling, and vascular smooth muscle cell contractility. Marfan syndrome, Loeys-Dietz syndrome, and nonsyndromic HTAD demonstrate how genetic mutations can disrupt the components that stabilize the aortic wall. These pathogenic mechanisms influence matrix organization, intracellular signaling, and the contractile machinery within the mechanically stressed proximal aorta. In this review, we summarize current mechanistic insights into the major forms of HTAD and discuss how new molecular and cellular concepts could influence surveillance, genetic counseling, and genotype-guided therapeutic strategies.

Indexed as

Aorta, ThoracicAortic Aneurysm, ThoracicSignal TransductionAnimalsDissection, Thoracic AortaExtracellular MatrixHumansLoeys-Dietz SyndromeMarfan Syndromeaortic aneurysm and dissectionendothelial dysfunctionextracellular matrixgenotype–phenotype correlationheritable thoracic aortic diseaseLoeys–Dietz syndromeMarfan syndromemechanotransductionsmooth muscle celltransforming growth factor-β signaling

Identifiers

PMID42193944
PMCPMC13204093

What OpenQuestion holds

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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.