Evidence map›Paper›PMID 40415469›Full record

ArticleClinical and translational medicine2025

CD248 deficiency promotes angiotensin II-induced aortic lesion by attenuating receptor stability in smooth muscle cells.

Tai-Tzu Hsieh, Ya-Chu Ku, Chu-Jen Chen, Cheng-Hsiang Kuo, Bi-Ing Chang, Chien-Hung Yu, Yi-Heng Li, Pei-Jane Tsai, Shu-Wha Lin, Hua-Lin Wu and 2 more

Abstract read
In one paragraph

Article in Clinical and translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

12 authors.

Tai-Tzu HsiehInstitute of Clinical Medicine, College of Medicine, National Cheng Kung University, Tainan, Taiwan, ROC.
Ya-Chu KuInstitute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan, ROC.
Chu-Jen ChenInstitute of Clinical Medicine, College of Medicine, National Cheng Kung University, Tainan, Taiwan, ROC.
Cheng-Hsiang KuoDepartment of Biochemistry and Molecular Biology, College of Medicine, National Cheng Kung University, Tainan, Taiwan, ROC.
Bi-Ing ChangDepartment of Biochemistry and Molecular Biology, College of Medicine, National Cheng Kung University, Tainan, Taiwan, ROC.
Chien-Hung YuInstitute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan, ROC.
Yi-Heng LiDepartment of Internal Medicine, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan, ROC.
Pei-Jane TsaiDepartment of Medical Laboratory Science and Biotechnology, College of Medicine, National Cheng Kung University, Tainan, Taiwan, ROC.
Shu-Wha LinDepartment of Clinical Laboratory Sciences and Medical Biotechnology, College of Medicine, National Taiwan University, Taipei, Taiwan, ROC.
Hua-Lin WuInstitute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan, ROC.
Chwan-Yau LuoDivision of Cardiovascular Surgery, Department of Surgery, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan, ROC.
Yau-Sheng TsaiInstitute of Clinical Medicine, College of Medicine, National Cheng Kung University, Tainan, Taiwan, ROC.ORCID 0000-0002-5560-2661

Funding

Kaohsiung Medical University Hospital KMUH111-1R26National Health Research Institutes NHRI-EX107-10511SINational Science and Technology Council, Taiwan 110-2314-B-037-144National Science and Technology Council, Taiwan 110-2320-B-006-017-MY3National Science and Technology Council, Taiwan 111-2314-B-037-021National Science and Technology Council, Taiwan 111-2320-B-006-022-MY3National Science and Technology Council, Taiwan 111-2320-B-006-047-MY3National Science and Technology Council, Taiwan 112-2314-B-037-106
6 · The paper itself

Abstract

backgroundAbdominal aortic aneurysm (AAA) is characterized by progressive dilation of the abdominal aorta that has a high prevalence of death due to aortic rupture. The hallmark of AAA is severe degeneration of the aortic media with the loss of vascular smooth muscle cells (VSMCs), the main source of extracellular matrix (ECM) proteins. CD248 was originally implicated in angiogenesis and tumourigenesis, but its role in the development of AAA remains unclear.

methodsMice lacking CD248 (Cd248

resultsCD248 expression was upregulated in the media and adventitia of patients and mice with aortic aneurysm. CD248 deficiency in mice exacerbates Ang II-induced aortic lesion along with severe disruption of elastic fibres and the VSMC layer. Interestingly, while compensatory ECM deposition was found in the aortic lesion of Cd248

conclusionsThe findings reveal that CD248 regulates the stability of the membrane receptors for Ang II and PDGF in VSMCs to transduce signals for collagen production in combating the loss of aortic wall strength during vascular remodelling. KEY POINTS: CD248 reduces the occurrence of angiotensin II (Ang II)-induced aortic lesion by facilitating collagen production to provide load-bearing properties to the aortic wall. CD248 regulates the stability of the membrane receptors for Ang II and PDGF in VSMCs. The C-terminal cytoplasmic tail of CD248 is a crucial domain that potentially regulates the stability of Ang II and PDGF receptors. This knowledge can enhance our understanding of how abdominal aortic aneurysm (AAA) can be treated through CD248-mediated signaling to maintain aortic wall strength during the remodeling process.

Indexed as

Angiotensin IIAntigens, CDAortic Aneurysm, AbdominalMyocytes, Smooth MuscleAnimalsDisease Models, AnimalHumansMaleMiceMice, Inbred C57BLMice, KnockoutMuscle, Smooth, VascularAngiotensin IIAntigens, CDangiotensin II receptorsaortic aneurysmCD248collagenPDGF receptorsvascular smooth muscle cells

Identifiers

PMID40415469
PMCPMC12104565

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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.