Evidence map›Paper›PMID 40801020›Full record

ArticleBioactive materials2025

Inhibition of ARH2 by pH/ROS-responsive nanosystem for improved lung adenocarcinoma immunochemotherapy.

Rui Cai, Meng Wang, Mengting Pan, Zhiwu Zhang, Qiang Jia, Longbao Feng, Zhongjian Yu, Lu Liu, Tongyu Zhu, Silin Cai and 4 more

Abstract read
In one paragraph

Article in Bioactive materials, 2025. 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

14 authors.

Rui CaiGuangzhou Institute of Cancer Research, The Affiliated Cancer Hospital, Guangzhou Medical University, Guangzhou, 510095, China.
Meng WangGuangzhou Institute of Cancer Research, The Affiliated Cancer Hospital, Guangzhou Medical University, Guangzhou, 510095, China.
Mengting PanGuangzhou Institute of Cancer Research, The Affiliated Cancer Hospital, Guangzhou Medical University, Guangzhou, 510095, China.
Zhiwu ZhangGuangzhou Institute of Cancer Research, The Affiliated Cancer Hospital, Guangzhou Medical University, Guangzhou, 510095, China.
Qiang JiaGuangzhou City Polytechnic, Guangzhou, 510405, China.
Longbao FengKey Laboratory of Biomaterials of Guangdong Higher Education Institutes, Guangdong Provincial Engineering and Technological Research Center for Drug Carrier Development, Department of Biomedical Engineering, Jinan University, Guangzhou, 510632, China.
Zhongjian YuGuangzhou Institute of Cancer Research, The Affiliated Cancer Hospital, Guangzhou Medical University, Guangzhou, 510095, China.
Lu LiuGuangzhou Institute of Cancer Research, The Affiliated Cancer Hospital, Guangzhou Medical University, Guangzhou, 510095, China.
Tongyu ZhuGuangzhou Institute of Cancer Research, The Affiliated Cancer Hospital, Guangzhou Medical University, Guangzhou, 510095, China.
Silin CaiGuangzhou Institute of Cancer Research, The Affiliated Cancer Hospital, Guangzhou Medical University, Guangzhou, 510095, China.
Han TianGuangzhou Institute of Cancer Research, The Affiliated Cancer Hospital, Guangzhou Medical University, Guangzhou, 510095, China.
Jiangyu ZhangGuangzhou Institute of Cancer Research, The Affiliated Cancer Hospital, Guangzhou Medical University, Guangzhou, 510095, China.
Rui GuoKey Laboratory of Biomaterials of Guangdong Higher Education Institutes, Guangdong Provincial Engineering and Technological Research Center for Drug Carrier Development, Department of Biomedical Engineering, Jinan University, Guangzhou, 510632, China.
Yanfang ZhengGuangzhou Institute of Cancer Research, The Affiliated Cancer Hospital, Guangzhou Medical University, Guangzhou, 510095, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immunotherapy resistance remains a substantial barrier to improving treatment outcomes for patients with lung adenocarcinoma (LUAD). Identifying effective immunotherapy target is crucial for enhancing therapeutic efficacy in LUAD. Through database analysis, we discovered that ADP ribosylhydrolase-like 1 (ADPRHL1, ARH2) is associated with immunosuppression. In this study, we first demonstrated that the increased presence of ARH2-positive macrophages in LUAD tumors is associated with immunosuppression. Furthermore, ARH2 promotes M2 macrophage polarization and suppresses immune responses by regulating the FPR2/PI3K/AKT signaling pathway. Additionally, we found that artesunate (ART) can induce necroptosis in LUAD cells and activate antitumor immune responses. To translate these findings into a clinically viable therapeutic approach, we developed a pH/ROS-responsive nanosystem capable of co-delivering siARH2 and ART. This nanosystem effectively activated immune responses in both tumor cells and tumor-associated macrophages. Furthermore, the nanosystem demonstrated excellent

Indexed as

ADP ribosylhydrolase-like 1 (ADPRHL1ARH2)Lung adenocarcinoma (LUAD)M2 macrophagesNecroptosispH/ROS-Responsive nanosystem

Identifiers

PMID40801020
PMCPMC12341593

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Registered trials

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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.