Evidence map›Paper›PMID 38261238›Full record

ArticleMolecular and cellular biochemistry2024

Apigenin accelerates wound healing in diabetic mice by promoting macrophage M2-type polarization via increasing miR-21 expression.

Ke Li, Lijun Wu, Jingting Jiang

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Article in Molecular and cellular biochemistry, 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
7.0field-weighted citation impact, top 3% 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, 28 citations in OpenAlex.

  1. ACS omega · 2026
    Article
  2. Review
  3. Article
  4. Article
  5. Food science & nutrition · 2026
    Review
  6. Review
  7. Article
  8. Article
  9. Polyphenols in wound healing: unlocking prospects with clinical applications.Naunyn-Schmiedeberg's archives of pharmacology · 2025
    Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. Article
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  19. 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

3 authors at 2 institutions in 1 country.

Ke Li *Jiangsu Engineering Research Center for Tumor Immunotherapy, The Third Affiliated Hospital of Soochow University, Changzhou, 213003, Jiangsu, China.
Lijun Wu *Department of Plastic and Aesthetic Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, 215006, Jiangsu, China.
Jingting JiangJiangsu Engineering Research Center for Tumor Immunotherapy, The Third Affiliated Hospital of Soochow University, Changzhou, 213003, Jiangsu, China. jiangjingting@suda.edu.cn.
Soochow University · CNFirst Affiliated Hospital of Soochow University · CN

Funding

Hospital Research Fund SDFEYBS1805Project of State Key Laboratory of Radiation Medicine and Protection, Soochow University GZK1202244Suzhou People's Livelihood Science and Technology Project SYS2020105Suzhou Science and Technology Development Project SYS2020105The Special Project of "Technological Innovation" Project of CNNC Medical Industry Co. Ltd ZHYLZD2021002
6 · The paper itself

Abstract

The alteration of inflammatory phenotype by macrophage polarization plays an important role in diabetic wound repair. Apigenin has been reported to be anti-inflammatory and promote tissue repair; however, whether it regulates macrophage polarization to participate in diabetic wound repair remains to be investigated. We found that apigenin promoted miR-21 expression in LPS-stimulated RAW264.7 cells, inhibited cellular M1-type factor TNF-α and IL-1β secretion and increased M2-type factor IL-10 and TGF-β secretion, and accelerated macrophage conversion from M1 type to M2 type, whereas this protective effect of apigenin was counteracted by a miR-21 inhibitor. Moreover, we established a macrophage-HUVECs cell in vitro co-culture system and found that apigenin accelerated the migration, proliferation, and VEGF secretion of HUVECs by promoting macrophage miR-21 expression. Further, mechanistic studies revealed that this was mediated by the TLR4/Myd88/NF-κB axis. In in vivo study, diabetic mice had significantly delayed wound healing compared to non-diabetic mice, accelerated wound healing in apigenin-treated diabetic mice, and decreased M1-type macrophages and increased M2-type macrophages in wound tissues.

Indexed as

ApigeninDiabetes Mellitus, ExperimentalMacrophagesMicroRNAsWound HealingAnimalsGene Expression RegulationHumansHuman Umbilical Vein Endothelial CellsMaleMiceRAW 264.7 CellsApigeninMicroRNAsMIRN21 microRNA, humanMIRN21 microRNA, mouseApigeninDiabetic wound healingMacrophagemiR-21

Identifiers

PMID38261238
OpenAlexW4391145103

What OpenQuestion holds

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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.