Evidence map›Paper›PMID 42226559›Full record

ArticleJournal of extracellular vesicles2026

Tumour-Derived Extracellular Vesicles Reprogramme Tumour-Associated Macrophages Into Immunosuppressive Phenotype via NOD1 Signalling in Clear Cell Renal Cell Carcinoma.

Xiu-Wu Pan, Mu-Chen Li, Tian-Yue Yang, Yi-Fan Liu, Jia-Lin Zhou, Yi-Fan Tang, Hong-Feng Zheng, Jian-Gui Liu, Zi-Chang Liu, Wen-Jie Ma and 17 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of extracellular vesicles, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

27 authors.

Xiu-Wu PanDepartment of Urology, Xinhua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Mu-Chen LiDepartment of Urology, Xinhua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Tian-Yue YangDepartment of Urology, Xinhua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Yi-Fan LiuDepartment of Urology, Xinhua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Jia-Lin ZhouDepartment of Urology, Xinhua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Yi-Fan TangDepartment of Urology, Xinhua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Hong-Feng ZhengDepartment of Urology, Xinhua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Jian-Gui LiuDepartment of Urology, Xinhua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Zi-Chang LiuDepartment of Urology, Xinhua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Wen-Jie MaDepartment of Urology, Xinhua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Wen-Yan LiDepartment of Urology, Xinhua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Zi-Xuan GongDepartment of Urology, Xinhua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Shun ZhangDepartment of Urology, Xinhua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Hang-Biao ZhangDepartment of Urology, Xinhua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Bing-Nan LuDepartment of Urology, Xinhua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Yun-Tao YaoDepartment of Urology, Xinhua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Dong-Hao LyuDepartment of Urology, Xinhua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Guan-Yu ZhuDepartment of Urology, Xinhua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Yuan-Bo ZongDepartment of Urology, Xinhua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Han-Lin YaoDepartment of Urology, Xinhua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Ai-Ping ZhangDepartment of Urology, Xinhua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Jin ZengDepartment of Urology, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China.
Si-Tu XiongDepartment of Urology, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China.
Ke-Qin DongDepartment of Urology, Xinhua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Wang ZhouDepartment of Urology, Xinhua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Bin FuDepartment of Urology, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China.
Xin-Gang CuiDepartment of Urology, Xinhua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.ORCID https://orcid.org/0000-0002-0920-9439

Funding

"Cross-Fund Project" of Xinhua Hospital JC2025G008National Key Research and Development Program of China 2024YFF1501304National Natural Science Foundation of China 82330094National Natural Science Foundation of China U25A20122Natural Science Foundation of Shanghai Municipality 23ZR1441300Shanghai Leading Talent Program Project LJ2024013Shanghai Oriental Talent Plan Youth Program QNJY2025090Shanghai Rising-Star Program 23QC1401400
6 · The paper itself

Abstract

Clear cell renal cell carcinoma (ccRCC)-derived extracellular vesicles (EVs) play a pivotal role in myeloid cell differentiation toward immunosuppressive phenotypes, yet the underlying mechanisms remain poorly understood. Through integrated single-nucleus RNA sequencing, EV proteomics, and phenotype validation, we identified NOD1, a pattern recognition receptor (PRR), as a critical mediator of EV-driven macrophage differentiation. Clinically, NOD1 overexpression in ccRCC tissues correlated with increased immunosuppressive macrophage infiltration, immune checkpoint inhibitors (ICIs) therapy resistance, and poor prognosis. Mechanistically, ccRCC-EVs enriched with SCRIB, a Rho GTPase activator, triggered sustained NOD1 activation in macrophages via Rho GTPase signalling. Crucially, NOD1 signalling converged on interferon regulatory factor 4 (IRF4), whose expression might be dynamically regulated through NF-κB activation and MITF suppression. Furthermore, inhibition of NOD1 promotes the therapeutic effect of ICIs in vivo. Our findings unveil a novel EV-mediated immune evasion mechanism in ccRCC and propose the SCRIB-NOD1-IRF4 axis as a therapeutic target to restore anti-tumour immunity.

Indexed as

Carcinoma, Renal CellExtracellular VesiclesKidney NeoplasmsNod1 Signaling Adaptor ProteinTumor-Associated MacrophagesAnimalsCell Line, TumorFemaleHumansInterferon Regulatory Factor-4Interferon Regulatory FactorsMicePhenotypeSignal TransductionInterferon Regulatory Factor-4Interferon Regulatory FactorsNOD1 protein, humanNod1 Signaling Adaptor Proteinclear cell renal cell carcinomaextracellular vesiclesIRF4NOD1 signallingSCRIB

Identifiers

PMID42226559
PMCPMC13239502

What Socratic 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 Socratic graph.