Evidence map›Paper›PMID 38691303›Full record

ArticleCardiovascular toxicology2024

Linarin Ameliorates Restenosis After Vascular Injury in Type 2 Diabetes Mellitus via Regulating ADAM10-Mediated Notch Signaling Pathway.

Aihua Jiang, Lin Liu, Jianping Wang, Yinglan Liu, Shanshan Deng, Tao Jiang

Abstract read
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Article in Cardiovascular toxicology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.3field-weighted citation impact, top 40% 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

2 citing papers in PubMed, 1 citations in OpenAlex.

  1. Review
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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

6 authors at 2 institutions in 1 country.

Aihua JiangDepartment of Endocrinology, The Second Affiliated Hospital, Hengyang Medical School, University of South China, No. 35 Jiefang Road, Zhengxiang District, Hengyang, 421001, Hunan Province, China.
Lin LiuDepartment of Gastroenterology, Hengyang Central Hospital, Hengyang, 421001, China.
Jianping WangDepartment of Endocrinology, The Second Affiliated Hospital, Hengyang Medical School, University of South China, No. 35 Jiefang Road, Zhengxiang District, Hengyang, 421001, Hunan Province, China.
Yinglan LiuDepartment of Endocrinology, The Second Affiliated Hospital, Hengyang Medical School, University of South China, No. 35 Jiefang Road, Zhengxiang District, Hengyang, 421001, Hunan Province, China.
Shanshan DengDepartment of Endocrinology, The Second Affiliated Hospital, Hengyang Medical School, University of South China, No. 35 Jiefang Road, Zhengxiang District, Hengyang, 421001, Hunan Province, China.
Tao JiangDepartment of Endocrinology, The Second Affiliated Hospital, Hengyang Medical School, University of South China, No. 35 Jiefang Road, Zhengxiang District, Hengyang, 421001, Hunan Province, China. qq505142506@163.com.
University of South China · CNHengyang Academy of Agricultural Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vascular lesions frequently arise as complication in patients diagnosed with diabetes mellitus (DM). Presently, percutaneous coronary intervention (PCI) and antithrombotic therapy serve as primary treatments. However, in-stent restenosis persists as a challenging clinical issue following PCI, lacking sustained and effective treatment. Linarin (LN) exhibits diverse pharmacological activities and is regarded as a potential drug for treating various diseases, including DM. But its specific role in restenosis after vascular injury in DM patients remains unclear. A rat model of diabetes-related restenosis was established to evaluate the role of LN on neointimal hyperplasia. Vascular smooth muscle cells (VSMCs) stimulated by high glucose (HG, 30 mM) underwent LN treatment. Additionally, an overexpression plasmid of A disintegrin and metalloproteinases (ADAM10) was constructed to transfect VSMCs. We employed CCK-8, Brdu, wound-healing scratch, and transwell migration assays to evaluate the proliferation and migration of VSMCs. Furthermore, western blot and immunofluorescence assays were utilized to investigate the expressions of ADAM10 and the downstream Notch signaling pathway in vivo and in vitro models. LN notably alleviated intimal hyperplasia after vascular injury in DM rats and reduced the protein expression of ADAM10, alongside its downstream Notch1 signaling pathway-related proteins (Notch1, NICD and Hes1) in rat carotid artery tissues. LN effectively suppressed the proliferation and migration of VSMCs induced by HG, downregulating the protein expression of ADAM10, Notch1, NICD and Hes1. Moreover, our findings indicated that ADAM10 overexpression significantly reversed LN's effects on proliferation, migration, and the expression of Notch1 signaling pathway-related proteins in HG-treated VSMCs. LN demonstrates potential therapeutic efficacy in addressing restenosis after diabetic-related vascular injury, with the ADAM10 mediated Notch signaling pathway playing a pivotal role.

Indexed as

ADAM10 ProteinAmyloid Precursor Protein SecretasesCarotid Artery InjuriesCell MovementCell ProliferationDiabetes Mellitus, ExperimentalMembrane ProteinsMuscle, Smooth, VascularMyocytes, Smooth MuscleNeointimaRats, Sprague-DawleySignal TransductionAnimalsCells, CulturedCoronary RestenosisDiabetes Mellitus, Type 2ADAM10 ProteinADAM10 protein, ratAmyloid Precursor Protein SecretasesMembrane ProteinsNotch1 protein, ratReceptor, Notch1Receptors, NotchTranscription Factor HES-1ADAM10LinarinNotch signaling pathwayRestenosis after vascular injuryType II diabetes mellitus

Identifiers

PMID38691303
OpenAlexW4396545346

What OpenQuestion holds

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Registered trials

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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.