Evidence map›Paper›PMID 38064164›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2024

An Autologous Macrophage-Based Phenotypic Transformation-Collagen Degradation System Treating Advanced Liver Fibrosis.

Bo-Wen Duan, Yan-Jun Liu, Xue-Na Li, Meng-Meng Han, Hao-Yuan Yu, He-Yuan Hong, Ling-Feng Zhang, Lei Xing, Hu-Lin Jiang

Open access · goldAbstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
6.7field-weighted citation impact, top 2% 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

19 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
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  9. Article
  10. Resveratrol ameliorates CClMolecular biology reports · 2025
    Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Macrophage heterogeneity in liver fibrosis.Frontiers in immunology · 2025
    Review
  19. 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

9 authors at 1 institution in 1 country.

Bo-Wen DuanState Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, 210009, China.
Yan-Jun LiuState Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, 210009, China.
Xue-Na LiState Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, 210009, China.
Meng-Meng HanState Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, 210009, China.
Hao-Yuan YuState Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, 210009, China.
He-Yuan HongState Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, 210009, China.
Ling-Feng ZhangState Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, 210009, China.
Lei XingState Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, 210009, China.
Hu-Lin JiangState Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, 210009, China.ORCID 0000-0002-1620-1777
China Pharmaceutical University · CN

Funding

Double First-class University Projects CPU2018GY06Double First-Rate construction plan of China Pharmaceutical University CPU2022QZ18National Key R&D Program of China 2022YFE0198400National Natural Science Foundation of China 82020108029National Natural Science Foundation of China 82073398Project of State Key Laboratory of Natural Medicines, China Pharmaceutical University SKLNMZZ202021
6 · The paper itself

Abstract

In advanced liver fibrosis (LF), macrophages maintain the inflammatory environment in the liver and accelerate LF deterioration by secreting proinflammatory cytokines. However, there is still no effective strategy to regulate macrophages because of the difficulty and complexity of macrophage inflammatory phenotypic modulation and the insufficient therapeutic efficacy caused by the extracellular matrix (ECM) barrier. Here, AC73 and siUSP1 dual drug-loaded lipid nanoparticle is designed to carry milk fat globule epidermal growth factor 8 (MFG-E8) (named MUA/Y) to effectively inhibit macrophage proinflammatory signals and degrade the ECM barrier. MFG-E8 is released in response to the high reactive oxygen species (ROS) environment in LF, transforming macrophages from a proinflammatory (M1) to an anti-inflammatory (M2) phenotype and inducing macrophages to phagocytose collagen. Collagen ablation increases AC73 and siUSP1 accumulation in hepatic stellate cells (HSCs) and inhibits HSCs overactivation. Interestingly, complete resolution of liver inflammation, significant collagen degradation, and HSCs deactivation are observed in methionine choline deficiency (MCD) and CCl

Indexed as

Liver CirrhosisMacrophagesCollagenHumansPhenotypeCollagenadvanced hepatic fibrosishepatic stellate cellsinflammationin situ collagen degradationlipid nanoparticlemacrophages

Identifiers

PMID38064164
PMCPMC10870050
OpenAlexW4389476564

What OpenQuestion 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 OpenQuestion graph.