Evidence map›Paper›PMID 39680681›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025

Hepatic Steatosis Aggravates Vascular Calcification via Extracellular Vesicle-Mediated Osteochondrogenic Switch of Vascular Smooth Muscle Cells.

Zhao-Lin Zeng, Zhi-Bo Zhao, Qing Yuan, Shi-Qi Yang, Zhen-Xing Wang, Zuo Wang, Shi-Yu Zeng, An-Qi Li, Qian Chen, Guo-Qiang Zhu and 7 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

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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

17 authors.

Zhao-Lin ZengDepartment of Metabolism and Endocrinology, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, 421001, P. R. China.
Zhi-Bo ZhaoDepartment of Metabolism and Endocrinology, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, 421001, P. R. China.
Qing YuanDepartment of Metabolism and Endocrinology, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, 421001, P. R. China.
Shi-Qi YangDepartment of Metabolism and Endocrinology, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, 421001, P. R. China.
Zhen-Xing WangDepartment of Orthopedics, Movement System Injury and Repair Research Center, National Clinical Research Center for Geriatric Disorders, Hunan Key Laboratory of Angmedicine, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, P. R. China.
Zuo WangInstitute of Cardiovascular Disease, Key Lab for Arteriosclerology of Hunan Province, Hengyang Medical School, University of South China, Hengyang, Hunan, 421001, P. R. China.
Shi-Yu ZengDepartment of Metabolism and Endocrinology, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, 421001, P. R. China.
An-Qi LiDepartment of Metabolism and Endocrinology, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, 421001, P. R. China.
Qian ChenDepartment of Metabolism and Endocrinology, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, 421001, P. R. China.
Guo-Qiang ZhuDepartment of Orthopedics, Movement System Injury and Repair Research Center, National Clinical Research Center for Geriatric Disorders, Hunan Key Laboratory of Angmedicine, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, P. R. China.
Xin-Hua XiaoDepartment of Metabolism and Endocrinology, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, 421001, P. R. China.
Guang-Hua LuoDepartment of Radiology, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, 421001, P. R. China.
Hai-Yan LuoDepartment of Gastroenterology, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, 421001, P. R. China.
Jiao-Yang LiDepartment of Occupational and Environmental Health, School of Public Health, Wuhan University, Wuhan, 430071, P. R. China.
Xu-Yu ZuDepartment of Metabolism and Endocrinology, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, 421001, P. R. China.
Hui XieDepartment of Orthopedics, Movement System Injury and Repair Research Center, National Clinical Research Center for Geriatric Disorders, Hunan Key Laboratory of Angmedicine, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, P. R. China.
Jiang-Hua LiuDepartment of Metabolism and Endocrinology, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, 421001, P. R. China.ORCID https://orcid.org/0000-0003-3010-5113

Funding

Clinical Research 4310 Program of the First Affiliated Hospital of the University of South China 20214310NHYCG02National Natural Science Foundation of China 82270939Natural Science Foundation of Hunan Province 2022JJ70036Postgraduate Scientific Research Innovation Project of Hunan Province CX20210917
6 · The paper itself

Abstract

The global incidence of metabolic dysfunction-associated fatty liver disease (MAFLD) has risen sharply. This condition is strongly associated with the risk of cardiovascular disease (CVD), but how MAFLD affects the development and progression of CVD, particularly concerning vascular calcification, remains unclear. Herein, extracellular vesicles (EVs) are identified from steatotic hepatocytes as a trigger that accelerated the progression of both vascular intimal and medial calcification. Steatotic hepatocytes are found to release more EVs, which are able to reach the vascular tissue, be taken up by vascular smooth muscle cells (VSMCs), and promote their osteogenic differentiation. Within these toxic vesicles, a protein cargo is identified called lectin galactoside-binding soluble 3 binding protein (Lgals3bp) that acted as a potent inducer of osteochondrogenic transformation in VSMCs. Both the inhibition of EV release and the liver-specific knockdown of Lgals3bp profoundly attenuated vascular calcification. This work partially explains the reason for the high incidence of vascular calcification in MAFLD and unveils a novel mechanism that may be used to prevent or treat cardiovascular complications in patients with MAFLD.

Indexed as

Extracellular VesiclesFatty LiverMuscle, Smooth, VascularMyocytes, Smooth MuscleOsteogenesisVascular CalcificationAnimalsHepatocytesHumansMaleMiceatherosclerosisextracellular vesiclesLgals3bpMAFLDvascular calcification

Identifiers

PMID39680681
PMCPMC11791995

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.