Evidence map›Paper›PMID 40791776›Full record

ArticleInternational journal of nanomedicine2025

Inhibition of Ferroptosis by Adipose Stem Cell-Derived Apoptotic Vesicles Enhances Angiogenesis and Accelerates Diabetic Wound Healing.

Jingyi Zhang, Jinxin Kuang, Shengkai Gong, Hanzhe Wang, Feng Ding, Lu Zhao, Lele Shi, Shiyu Liu, Yimin Zhao, Jiani Liu and 1 more

Abstract read
In one paragraph

Article in International journal of nanomedicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Article
  2. Integrated OAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. 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

11 authors.

Jingyi Zhang *State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, School of Stomatology, The Fourth Military Medical University, Xi'an, Shaanxi, 710032, People's Republic of China.ORCID 0009-0002-4697-3863
Jinxin Kuang *State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, School of Stomatology, The Fourth Military Medical University, Xi'an, Shaanxi, 710032, People's Republic of China.
Shengkai Gong *State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, School of Stomatology, The Fourth Military Medical University, Xi'an, Shaanxi, 710032, People's Republic of China.
Hanzhe WangState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, School of Stomatology, The Fourth Military Medical University, Xi'an, Shaanxi, 710032, People's Republic of China.
Feng DingState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, School of Stomatology, The Fourth Military Medical University, Xi'an, Shaanxi, 710032, People's Republic of China.
Lu ZhaoState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, School of Stomatology, The Fourth Military Medical University, Xi'an, Shaanxi, 710032, People's Republic of China.
Lele ShiState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, School of Stomatology, The Fourth Military Medical University, Xi'an, Shaanxi, 710032, People's Republic of China.ORCID 0009-0006-8385-3325
Shiyu LiuState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, School of Stomatology, The Fourth Military Medical University, Xi'an, Shaanxi, 710032, People's Republic of China.
Yimin ZhaoState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, School of Stomatology, The Fourth Military Medical University, Xi'an, Shaanxi, 710032, People's Republic of China.
Jiani LiuState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, School of Stomatology, The Fourth Military Medical University, Xi'an, Shaanxi, 710032, People's Republic of China.
Geng DouState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, School of Stomatology, The Fourth Military Medical University, Xi'an, Shaanxi, 710032, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Purpose: Impaired angiogenesis is a critical challenge in diabetic wound healing. While apoptotic derivatives of stem cells hold promise for regenerative therapy, their role in modulating angiogenesis within the diabetic wound microenvironment remains underexplored. This study aims to investigate whether adipose stem cell-derived apoptotic vesicles (ASCs-apoVs) promote angiogenesis and accelerate diabetic wound healing by inhibiting endothelial cell ferroptosis. Methods: Diabetic mice model was established by feeding with high-fat diet (HFD) for 3 months followed by full-thickness skin wound preparation. Adipose stem cells (ASCs) isolated from adipose tissue were treated with staurosporine (STS) to induce apoptosis in vitro. Apoptotic vesicles (apoVs) were isolated by differential centrifugation, characterized using TEM, dynamic light scattering (DLS), and Western blot, and applied topically to diabetic wounds. The therapeutic effects of apoVs on wound healing efficiency, vascularization level and endothelial cell ferroptosis were evaluated. Results: HFD-induced diabetes promoted lipid peroxidation (4HNE accumulation) and ferroptosis in endothelial cells (ECs), leading to reduced CD31 Conclusion: Ferroptosis of endothelial cells contributes to impaired vascularization in diabetic wounds. ApoVs represent a promising cell-free therapeutic approach to mitigate ferroptosis, restore endothelial function and promote angiogenesis, offering a potential strategy for diabetic wound management.

Indexed as

Diabetes Mellitus, ExperimentalExtracellular VesiclesFerroptosisNeovascularization, PhysiologicStem CellsWound HealingAdipose TissueAngiogenesisAnimalsApoptosisDiet, High-FatEndothelial CellsHumansLipid PeroxidationMaleMiceadipose stem cellsapoptotic vesiclesendothelial cellsferroptosisvascularizationwound healing

Identifiers

PMID40791776
PMCPMC12336384

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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.