Evidence map›Paper›PMID 40645963›Full record

ArticleNature communications2025

A programmable platelet theranostic platform for adaptive multi-stage delivery and synergistic immunotherapy in atherosclerosis.

Yi Li, Xueping Li, Ting Chen, Jian Li, Ji Qi, Wen Li

Abstract read
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Review
  2. Nanomaterials-Based Immunotherapy for Atherosclerosis.Small (Weinheim an der Bergstrasse, Germany) · 2026
    Review
  3. Article
  4. Review
  5. 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

6 authors.

Yi LiState Key Laboratory of Advanced Medical Materials and Devices, Tianjin Key Laboratory of Biomedical Materials and Key Laboratory of Biomaterials and Nanotechnology for Cancer Immunotherapy, Institute of Biomedical Engineering, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin, China.
Xueping LiState Key Laboratory of Advanced Medical Materials and Devices, Tianjin Key Laboratory of Biomedical Materials and Key Laboratory of Biomaterials and Nanotechnology for Cancer Immunotherapy, Institute of Biomedical Engineering, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin, China.
Ting ChenState Key Laboratory of Advanced Medical Materials and Devices, Tianjin Key Laboratory of Biomedical Materials and Key Laboratory of Biomaterials and Nanotechnology for Cancer Immunotherapy, Institute of Biomedical Engineering, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin, China.
Jian LiState Key Laboratory of Advanced Medical Materials and Devices, Tianjin Key Laboratory of Biomedical Materials and Key Laboratory of Biomaterials and Nanotechnology for Cancer Immunotherapy, Institute of Biomedical Engineering, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin, China.
Ji QiState Key Laboratory of Medicinal Chemical Biology, Key Laboratory of Bioactive Materials, Ministry of Education, Frontiers Science Center for Cell Responses, and College of Life Sciences, Nankai University, Tianjin, China. qiji@nankai.edu.cn.ORCID http://orcid.org/0000-0001-7597-9725
Wen LiState Key Laboratory of Advanced Medical Materials and Devices, Tianjin Key Laboratory of Biomedical Materials and Key Laboratory of Biomaterials and Nanotechnology for Cancer Immunotherapy, Institute of Biomedical Engineering, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin, China. liwen@bme.pumc.edu.cn.ORCID http://orcid.org/0000-0001-6783-1464

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macrophages, along with the inflammatory and maladaptive immune responses they trigger, play crucial roles in the progression and rupture of atherosclerosis. We develop an adaptable platelet-protein platform tailored for the targeted delivery of both antioxidant nanocatalysts and TRAF6 inhibitor to advance synergistic therapy for atherosclerosis. The platform is constructed by assembling nanocatalyst- and TRAF6 inhibitor-loaded protein clusters with reactive oxygen species-cleavable linkers, then anchoring them onto the platelet surface for guided delivery to atherosclerotic plaques. Upon entering the reactive oxygen species-rich microenvironment, the platform disintegrates into ultra-small protein blocks, facilitating plaque penetration and selective macrophage internalization. The Mn-based nanocatalyst effectively scavenges various reactive oxygen species, while Mn ions concurrently enhance T1-weighted magnetic resonance imaging signals for diagnosis of atherosclerotic plaques. Meanwhile, the TRAF6 inhibitor blocks macrophage activation mediated by T lymphocytes. In a male mouse model of atherosclerosis, the versatile platform integrates cell-mediated natural targeting with adaptable size transformation for enhanced intraplaque penetration and unfavorable macrophage signaling reprogramming, offering opportunities for precise and multifaceted atherosclerosis therapy.

Indexed as

AtherosclerosisBlood PlateletsDrug Delivery SystemsImmunotherapyTheranostic NanomedicineAnimalsAntioxidantsDisease Models, AnimalHumansMacrophage ActivationMacrophagesMagnetic Resonance ImagingMaleMiceMice, Inbred C57BLPlaque, AtheroscleroticAntioxidantsReactive Oxygen SpeciesTNF Receptor-Associated Factor 6

Identifiers

PMID40645963
PMCPMC12254273

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.