Evidence map›Paper›PMID 36675309›Full record

ReviewInternational journal of molecular sciences2023

Molecular Mechanisms in Genetic Aortopathy-Signaling Pathways and Potential Interventions.

Charlotte Xue Dong, Cassandra Malecki, Elizabeth Robertson, Brett Hambly, Richmond Jeremy

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2023. 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
–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

15 citing papers in PubMed.

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  9. Attenuation of PI3K/AKT signaling pathway byBiochemistry and biophysics reports · 2024
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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

5 authors.

Charlotte Xue DongFaculty of Health and Medical Sciences, University of Sydney, Sydney, NSW 2006, Australia.ORCID 0000-0002-2726-4968
Cassandra MaleckiFaculty of Health and Medical Sciences, University of Sydney, Sydney, NSW 2006, Australia.ORCID 0000-0002-2367-9541
Elizabeth RobertsonFaculty of Health and Medical Sciences, University of Sydney, Sydney, NSW 2006, Australia.
Brett HamblyFaculty of Health and Medical Sciences, University of Sydney, Sydney, NSW 2006, Australia.ORCID 0000-0002-5988-562X
Richmond JeremyFaculty of Health and Medical Sciences, University of Sydney, Sydney, NSW 2006, Australia.ORCID 0000-0003-1281-0505

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Thoracic aortic disease affects people of all ages and the majority of those aged <60 years have an underlying genetic cause. There is presently no effective medical therapy for thoracic aneurysm and surgery remains the principal intervention. Unlike abdominal aortic aneurysm, for which the inflammatory/atherosclerotic pathogenesis is well established, the mechanism of thoracic aneurysm is less understood. This paper examines the key cell signaling systems responsible for the growth and development of the aorta, homeostasis of endothelial and vascular smooth muscle cells and interactions between pathways. The evidence supporting a role for individual signaling pathways in pathogenesis of thoracic aortic aneurysm is examined and potential novel therapeutic approaches are reviewed. Several key signaling pathways, notably TGF-β, WNT, NOTCH, PI3K/AKT and ANGII contribute to growth, proliferation, cell phenotype and survival for both vascular smooth muscle and endothelial cells. There is crosstalk between pathways, and between vascular smooth muscle and endothelial cells, with both synergistic and antagonistic interactions. A common feature of the activation of each is response to injury or abnormal cell stress. Considerable experimental evidence supports a contribution of each of these pathways to aneurysm formation. Although human information is less, there is sufficient data to implicate each pathway in the pathogenesis of human thoracic aneurysm. As some pathways i.e., WNT and NOTCH, play key roles in tissue growth and organogenesis in early life, it is possible that dysregulation of these pathways results in an abnormal aortic architecture even in infancy, thereby setting the stage for aneurysm development in later life. Given the fine tuning of these signaling systems, functional polymorphisms in key signaling elements may set up a future risk of thoracic aneurysm. Multiple novel therapeutic agents have been developed, targeting cell signaling pathways, predominantly in cancer medicine. Future investigations addressing cell specific targeting, reduced toxicity and also less intense treatment effects may hold promise for effective new medical treatments of thoracic aortic aneurysm.

Indexed as

Aortic Aneurysm, AbdominalAortic Aneurysm, ThoracicEndothelial CellsHumansMyocytes, Smooth MusclePhosphatidylinositol 3-KinasesSignal TransductionPhosphatidylinositol 3-KinasesaneurysmaortaendotheliumMarfanvascular smooth muscle

Identifiers

PMID36675309
PMCPMC9865322

What Socratic 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 Socratic graph.