Evidence map›Paper›PMID 41993636›Full record

ArticleTheranostics2026

Macrophage membrane-biomimetic cinnamaldehyde nanomedicine ameliorates inflammatory bowel disease by suppressing macrophage M1 polarization.

Zebin Huang, Lingna Xie, Qi Shu, Yongyu Xu, Xiao-Chun Guo, Shimin Wang, Shuyi Li, Yaoxun Zeng, Xiu-Cai Chen, Mingtao Huang and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Theranostics, 2026. 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

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

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

12 authors.

Zebin HuangSchool of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou, China.
Lingna XieSchool of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou, China.
Qi ShuSchool of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou, China.
Yongyu XuSchool of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou, China.
Xiao-Chun GuoSchool of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou, China.
Shimin WangSchool of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou, China.
Shuyi LiSchool of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou, China.
Yaoxun ZengSchool of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou, China.
Xiu-Cai ChenSchool of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou, China.
Mingtao HuangSchool of Food Science and Engineering, South China University of Technology, Guangzhou, China.
Fujun JinSchool of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou, China.
Yu-Jing LuSchool of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rationale: Inflammatory bowel disease (IBD), known for its complexity and frequent relapses, urgently demands novel therapeutics due to the limited efficacy of current treatments. Cinnamaldehyde (CMA), a bioactive compound derived from Methods: Using RAW 264.7 cells stimulated with either LPS or IL-4, we evaluated the effects of CMA on macrophage polarization. Subsequently, the impact of CMA on glucose metabolism in M1 macrophages was analyzed. RNA sequencing identified the signaling pathways through which CMA inhibits M1 macrophage polarization, and this was further validated through genetic or pharmacological blockade. To overcome the pharmacokinetic challenges of CMA, macrophage membrane-biomimetic CMA-loaded nanoparticles (MM@CMANP) were designed, and their pharmacokinetics and targeting to intestinal inflammation sites were evaluated. Finally, the efficacy of MM@CMANP was assessed in DSS-induced IBD mice. Results: CMA suppresses M1 macrophage polarization Conclusions: These results establish mitophagy as a central mechanism underlying anti-IBD effects of CMA and position MM@CMANP as a clinically translatable nanotherapeutic platform for IBD.

Indexed as

AcroleinInflammatory Bowel DiseasesMacrophagesAnimalsDisease Models, AnimalGlucoseMacrophage ActivationMembrane ProteinsMiceMice, Inbred C57BLMitochondrial ProteinsMitophagyNanomedicineNanoparticlesRAW 264.7 CellsAcroleinBNip3 protein, mousecinnamaldehydeGlucoseMembrane ProteinsMitochondrial ProteinscinnamaldehydeIBDmacrophage membrane-biomimetic nanoplatformmacrophage polarizationmitophagy

Identifiers

PMID41993636
PMCPMC13080821

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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.