Evidence map›Paper›PMID 41501766›Full record

ArticleJournal of nanobiotechnology2026

A novel protein B2URF3 from Akkermansia muciniphila increased by intermittent fasting alleviates vascular calcification.

Shi-Yu Zeng, Jiang-Hua Liu, Ying-Ying Xiang, Zhao-Lin Zeng, Zhi-Bo Zhao, Jie Zheng, Yi-Fu Liu, Zhi-Rou Lin, Yi-Yi Wang, Chun-Gu Hong and 10 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of nanobiotechnology, 2026. 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
–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

2 citing papers in PubMed.

  1. Review
  2. Article
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.

Shi-Yu ZengDepartment of Metabolism and Endocrinology, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, 421001, Hunan, China.
Jiang-Hua LiuDepartment of Orthopedics, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, 421001, Hunan, China.
Ying-Ying XiangDepartment of Metabolism and Endocrinology, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, 421001, Hunan, China.
Zhao-Lin ZengDepartment of Metabolism and Endocrinology, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, 421001, Hunan, China.
Zhi-Bo ZhaoDepartment of Metabolism and Endocrinology, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, 421001, Hunan, China.
Jie ZhengDepartment of Metabolism and Endocrinology, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, 421001, Hunan, China.
Yi-Fu LiuDepartment of Urology, The Second Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, China.
Zhi-Rou LinDepartment of Metabolism and Endocrinology, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, 421001, Hunan, China.
Yi-Yi WangDepartment of Orthopedics, Movement System Injury and Repair Research Center, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Chun-Gu HongDepartment of Orthopedics, Movement System Injury and Repair Research Center, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Ling JinDepartment of Orthopedics, Movement System Injury and Repair Research Center, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Guo-Qiang ZhuDepartment of Orthopedics, Movement System Injury and Repair Research Center, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Yi-Wei LiuDepartment of Orthopedics, Movement System Injury and Repair Research Center, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Xin WangDepartment of Orthopedics, Movement System Injury and Repair Research Center, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Xiao-Xue LiDepartment of Orthopedics, Movement System Injury and Repair Research Center, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Zhe GuanDepartment of Orthopedics, Movement System Injury and Repair Research Center, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Zhen-Xing WangDepartment of Orthopedics, Movement System Injury and Repair Research Center, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Ting SunDepartment of Urology, The First Affiliated Hospital of Nanchang University, Nanchang, 330000, Jiangxi, China.
Hui XieDepartment of Orthopedics, Movement System Injury and Repair Research Center, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China. huixie@csu.edu.cn.
Jiang-Hua LiuDepartment of Metabolism and Endocrinology, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, 421001, Hunan, China. liujianghua@usc.edu.cn.

Funding

Natural Science Foundation of Hunan Province 2022JJ70036the Clinical Rsearch 4310 Program of the First Affiliated Hospotal of the University of South China 20214310NHYCG02the National Natural Science Foundation of China 82270939
6 · The paper itself

Abstract

Vascular calcification (VC) is a major contributor to cardiovascular morbidity and mortality, yet effective therapies are lacking. Here, we show that alternate-day intermittent fasting (IF1:1) attenuates vitamin D-induced VC in mice, whereas a 5:2 regimen is ineffective. The protective effect of IF1:1 is gut microbiota-dependent, particularly through enrichment of Akkermansia muciniphila (Akk). Microbiota-derived extracellular vesicles (EVs) function as nano-scale mediators that bypass the spatiotemporal constraints of bacterial survival to facilitate long-distance communication with host cells, providing a crucial pathway for downstream mechanistic investigation. Akk-derived EVs (Akk-EVs) are internalized by vascular smooth muscle cells (VSMCs), suppressing osteogenic differentiation and calcification in vitro and in vivo. Proteomic analysis identified B2URF3 as a highly enriched functional protein in Akk-EVs and Akk, which interacts with Aldehyde Dehydrogenase 1 Family Member B1 (ALDH1B1) to inhibit VSMC osteogenic transdifferentiation. Clinically, reduced fecal Akk abundance and lower serum B2URF3 levels were observed in patients with coronary calcification. These findings define a gut-vascular axis by which IF1:1 mitigates VC and nominate Akk-EVs and B2URF3 as potential therapeutic targets and biomarkers.

Indexed as

Bacterial ProteinsVascular CalcificationAkkermansiaAnimalsExtracellular VesiclesGastrointestinal MicrobiomeHumansIntermittent FastingMaleMiceMice, Inbred C57BLMuscle, Smooth, VascularMyocytes, Smooth MuscleOsteogenesisVerrucomicrobiaBacterial ProteinsAkkermansia muciniphilaExtracellular vesiclesGut-vascular axisIntermittent fastingVascular calcification

Identifiers

PMID41501766
PMCPMC12781770

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.