Evidence map›Paper›PMID 41492458›Full record

ArticleJournal of pharmaceutical analysis2025

Targeted reduction-responsive nanovehicles for photodynamic therapy-primed immunotherapy in melanoma.

Chenqian Feng, Lingfeng Zhou, Bo Chen, Hui Li, Min Mu, Rangrang Fan, Haifeng Chen, Gang Guo

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of pharmaceutical analysis, 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

8 authors.

Chenqian FengState Key Laboratory of Biotherapy and Cancer Center, Department of Neurosurgery, West China Hospital, Sichuan University, Chengdu, 610041, China.
Lingfeng ZhouState Key Laboratory of Biotherapy and Cancer Center, Department of Neurosurgery, West China Hospital, Sichuan University, Chengdu, 610041, China.
Bo ChenState Key Laboratory of Biotherapy and Cancer Center, Department of Neurosurgery, West China Hospital, Sichuan University, Chengdu, 610041, China.
Hui LiState Key Laboratory of Biotherapy and Cancer Center, Department of Neurosurgery, West China Hospital, Sichuan University, Chengdu, 610041, China.
Min MuState Key Laboratory of Biotherapy and Cancer Center, Department of Neurosurgery, West China Hospital, Sichuan University, Chengdu, 610041, China.
Rangrang FanDepartment of Neurosurgery and Institute of Neurosurgery, West China Hospital, Sichuan University, Chengdu, 610041, China.
Haifeng ChenDepartment of Neurosurgery and Institute of Neurosurgery, West China Hospital, Sichuan University, Chengdu, 610041, China.
Gang GuoState Key Laboratory of Biotherapy and Cancer Center, Department of Neurosurgery, West China Hospital, Sichuan University, Chengdu, 610041, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Melanoma, a common malignant skin tumor, faces challenges with multidrug resistance and high recurrence rates. Combining photodynamic therapy (PDT) and immunotherapy offers a promising personalized treatment approach. However, poor water solubility and significant side effects of photosensitizers and immune checkpoint inhibitors (ICIs) limit their application. Enhancing delivery efficiency while reducing adverse effects is crucial. Herein, we formulate BM@HSSC nanoparticles (NPs), which consist of a reduction-responsive hyaluronic acid (HA) backbone modified with photosensitizer chlorin e6 (Ce6) and loaded with the programmed cell death-ligand 1 (PD-L1) inhibitor BMS-1. This system synergistically integrates PDT, immunogenic cell death (ICD), and immunotherapy for melanoma treatment. BM@HSSC NPs target and accumulate at the tumor site via the CD44 receptor. The disulfide bonds (-S-S-) in the NPs react with high glutathione (GSH) concentrations in tumor cells, rapidly releasing Ce6 and BMS-1. Under 660 nm laser irradiation, BM@HSSC NPs generate cytotoxic reactive oxygen species (ROS), inducing cell apoptosis and triggering ICD via PDT damage-associated molecular patterns (DAMPs) and tumor-associated antigens (TAAs) released from ICD promote dendritic cell (DC) maturation, enhancing antigen presentation and activating cytotoxic T lymphocytes (CTLs). Meanwhile, BMS-1 blocks the programmed cell death-1 (PD-1)/PD-L1 pathway, countering the immunosuppressive tumor microenvironment (iTME) and inhibiting tumor cell immune escape. This strategy amplifies antitumor immune responses by enhancing immunogenicity and synergizing with ICIs, resulting in robust antitumor efficacy.

Indexed as

Hyaluronic acidImmune checkpoint blockadeImmunogenic cell deathPhotodynamic therapyReduction responsive

Identifiers

PMID41492458
PMCPMC12765061

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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.