Evidence map›Paper›PMID 38432393›Full record

ArticleJournal of advanced research2025

Moscatilin inhibits vascular calcification by activating IL13RA2-dependent inhibition of STAT3 and attenuating the WNT3/β-catenin signalling pathway.

Tingting Zhang, Mengmeng Zhu, Jialing Ma, Zhenghong Liu, Zhidan Zhang, Meijie Chen, Yaping Zhao, Huaxin Li, Shengnan Wang, Xiaoning Wei and 10 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of advanced research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
5.3field-weighted citation impact, top 4% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.

  1. Merits of bioactivity and products ofFrontiers in plant science · 2026
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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

20 authors at 7 institutions in 3 countries.

Tingting ZhangKey Laboratory of Major Metabolic Diseases and Nutritional Regulation of Anhui Department of Education, Anhui Provincial International Science and Technology Cooperation Base for Major Metabolic Diseases and Nutritional Interventions, School of Food and Biological Engineering, Hefei University of Technology, Hefei, China.
Mengmeng ZhuKey Laboratory of Major Metabolic Diseases and Nutritional Regulation of Anhui Department of Education, Anhui Provincial International Science and Technology Cooperation Base for Major Metabolic Diseases and Nutritional Interventions, School of Food and Biological Engineering, Hefei University of Technology, Hefei, China.
Jialing MaKey Laboratory of Major Metabolic Diseases and Nutritional Regulation of Anhui Department of Education, Anhui Provincial International Science and Technology Cooperation Base for Major Metabolic Diseases and Nutritional Interventions, School of Food and Biological Engineering, Hefei University of Technology, Hefei, China.
Zhenghong LiuDepartment of Endocrinology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.
Zhidan ZhangDepartment of Endocrinology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.
Meijie ChenDepartment of Endocrinology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.
Yaping ZhaoDepartment of Endocrinology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.
Huaxin LiKey Laboratory of Major Metabolic Diseases and Nutritional Regulation of Anhui Department of Education, Anhui Provincial International Science and Technology Cooperation Base for Major Metabolic Diseases and Nutritional Interventions, School of Food and Biological Engineering, Hefei University of Technology, Hefei, China.
Shengnan WangKey Laboratory of Major Metabolic Diseases and Nutritional Regulation of Anhui Department of Education, Anhui Provincial International Science and Technology Cooperation Base for Major Metabolic Diseases and Nutritional Interventions, School of Food and Biological Engineering, Hefei University of Technology, Hefei, China.
Xiaoning WeiKey Laboratory of Major Metabolic Diseases and Nutritional Regulation of Anhui Department of Education, Anhui Provincial International Science and Technology Cooperation Base for Major Metabolic Diseases and Nutritional Interventions, School of Food and Biological Engineering, Hefei University of Technology, Hefei, China.
Wenwen ZhangTianjin Central Hospital of Obstetrics and Gynecology, Tianjin, China.
Xiaoxiao YangKey Laboratory of Major Metabolic Diseases and Nutritional Regulation of Anhui Department of Education, Anhui Provincial International Science and Technology Cooperation Base for Major Metabolic Diseases and Nutritional Interventions, School of Food and Biological Engineering, Hefei University of Technology, Hefei, China.
Peter J LittleSchool of Pharmacy, Pharmacy Australia Centre of Excellence, The University of Queensland, Woolloongabba, Queensland 4102, Australia.
Danielle KamatoDiscovery Biology, Griffith Institute for Drug Discovery, Griffith University, Nathan, Queensland 4111, Australia.
Hao HuDepartment of Cardiology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.
Yajun DuanDepartment of Cardiology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.
Baotong ZhangDepartment of Human Cell Biology and Genetics, School of Medicine, Southern University of Science and Technology, Shenzhen 518055, China.
Jianbo XiaoDepartment of Analytical and Food Chemistry, Faculty of Sciences, Universidade de Vigo, Nutrition and Bromatology Group, Ourense, Spain.
Suowen XuDepartment of Endocrinology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China. Electronic address: sxu1984@ustc.edu.cn.
Yuanli ChenKey Laboratory of Major Metabolic Diseases and Nutritional Regulation of Anhui Department of Education, Anhui Provincial International Science and Technology Cooperation Base for Major Metabolic Diseases and Nutritional Interventions, School of Food and Biological Engineering, Hefei University of Technology, Hefei, China. Electronic address: chenyuanli@hfut.edu.cn.
Anhui University · CNUniversity of Science and Technology of China · CNGriffith University · AUSouthern University of Science and Technology · CNThe University of Queensland · AUTianjin Central Hospital of Gynecology Obstetrics · CNUniversidade de Vigo · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionVascular calcification, a devastating vascular complication accompanying atherosclerotic cardiovascular disease and chronic kidney disease, increases the incidence of adverse cardiovascular events and compromises the efficacy of vascular interventions. However, effective therapeutic drugs and treatments to delay or prevent vascular calcification are lacking.

objectivesThis study was designed to test the therapeutic effects and mechanism of Moscatilin (also known as dendrophenol) from Dendrobium huoshanense (an eminent traditional Chinese medicine) in suppressing vascular calcification in vitro, ex vivo and in vivo.

methodsMale C57BL/6J mice (25-week-old) were subjected to nicotine and vitamin D

resultsBy utilizing an in-house drug screening strategy, we identified Moscatilin as a new naturally-occurring chemical entity to reduce HASMC calcium accumulation. The protective effects of Moscatilin against vascular calcification were verified in cultured HASMCs. Unbiased transcriptional profiling analysis and cellular thermal shift assay suggested that Moscatilin suppresses vascular calcification via binding to interleukin 13 receptor subunit A2 (IL13RA2) and augmenting its expression. Furthermore, IL13RA2 was reduced during HASMC osteogenesis, thus promoting the secretion of inflammatory factors via STAT3. We further validated the participation of Moscatilin-inhibited vascular calcification by the classical WNT/β-catenin pathway, among which WNT3 played a key role in this process. Moscatilin mitigated the crosstalk between WNT3/β-catenin and IL13RA2/STAT3 to reduce osteogenic differentiation of HASMCs.

conclusionThis study supports the potential of Moscatilin as a new naturally-occurring candidate drug for treating vascular calcification via regulating the IL13RA2/STAT3 and WNT3/β-catenin signalling pathways.

Indexed as

STAT3 Transcription FactorVascular CalcificationWnt Signaling PathwayAnimalsbeta CateninCells, CulturedDisease Models, AnimalHumansMaleMiceMice, Inbred C57BLMuscle, Smooth, VascularMyocytes, Smooth MuscleOsteogenesisbeta CateninStat3 protein, mouseSTAT3 Transcription FactorDendrophenolIL13RΑ2MoscatilinSTAT3Vascular calcificationWNT3β-catenin

Identifiers

PMID38432393
PMCPMC11785559
OpenAlexW4392613608

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.