Evidence map›Paper›PMID 41021282›Full record

ArticleHepatology communications2025

TNAP-induced CD47 membrane expression enhances TGF-β1 conversion in liver fibrosis.

Lei Gao, Fengling Peng, Peng Qi, Hanqiu Zhang, Hao Chi, Liang Deng, Xin Liang, Min Sun, Wenkun Ma, Cheng Yang and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

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

0numbers the graph read from it
0cells of the map it votes in
1citing 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

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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

1 citing paper in PubMed.

  1. Review
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

14 authors.

Lei GaoDepartment of Cardiovascular Medicine, Cardiovascular Research Center, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.ORCID 0000-0002-7972-2908
Fengling PengDepartment of Infectious Disease, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Peng QiDepartment of Infectious Disease, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Hanqiu ZhangDepartment of Quantitative Health Sciences, John A. Burns School of Medicine, University of Hawaii at Manoa, Honolulu, Hawaii, USA.
Hao ChiClinical Medical College, Southwest Medical University, Sichuan, China.
Liang DengDepartment of Gastroenterology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Xin LiangDepartment of Pathology, School of Basic Medical Sciences, Chongqing Medical University, Chongqing, China.
Min SunHealth Management Center, The First Branch of the Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Wenkun MaJames L. Winkle College of Pharmacy, University of Cincinnati, Cincinnati, Ohio, USA.
Cheng YangDepartment of Infectious Disease, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Qiang LiuDepartment of Hepatological Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Xiaoyu WeiDepartment of Infectious Disease, The Affiliated Yongchuan Hospital of Chongqing Medical University, Chongqing, China.
Yongguo LiDepartment of Infectious Disease, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Jinqiu ZhaoDepartment of Infectious Disease, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTissue-nonspecific alkaline phosphatase (TNAP) expression increases after liver injury, but its role in liver fibrosis remains unclear. This study investigated the effect of TNAP on liver fibrosis and its mechanism in regulating TGF-β1 signaling.

methodsHuman liver samples and a CCl4-induced liver fibrosis mouse model with adv-TNAP and a TNAP inhibitor (tetramisole, Tetra) were used to study the function of TNAP in liver fibrosis. Primary HSCs were used to study the mechanism of TNAP in regulating the TGF-β1 signal.

resultsElevated TNAP expression was observed in human and murine fibrotic liver tissues, correlating with increased fibrotic markers. In vivo experiments using TNAP overexpression and inhibition in a CCl4-induced liver fibrosis mouse model demonstrated that TNAP exacerbated, while its inhibition alleviated, liver fibrosis. In vitro studies revealed that TNAP regulated TGF-β1 conversion and HSCs activation through the TGF-β1/SMAD pathway. TNAP facilitated TGF-β1 conversion by promoting the interaction between CD47 and thrombospondin-1 (TSP1). Membrane expression of CD47 modulated by TNAP might contribute to the binding effect of CD47 and TSP1.

conclusionsTNAP plays a critical regulatory role in TGF-β1-mediated liver fibrosis, probably by promoting the binding of CD47/TSP1. Targeting TNAP-mediated pathways may offer new therapeutic strategies for liver fibrosis.

Indexed as

Alkaline PhosphataseCD47 AntigenLiver CirrhosisTransforming Growth Factor beta1AnimalsCarbon TetrachlorideDisease Models, AnimalHepatic Stellate CellsHumansLiverMaleMiceMice, Inbred C57BLSignal TransductionThrombospondin 1Alkaline PhosphataseCarbon TetrachlorideCD47 AntigenCD47 protein, humanTGFB1 protein, humanThrombospondin 1thrombospondin-1, humanTransforming Growth Factor beta1CD47liver fibrosisTGF-β1 conversionTNAP

Identifiers

PMID41021282
PMCPMC12483068

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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.