Evidence map›Paper›PMID 38453925›Full record

ArticleSignal transduction and targeted therapy2024

Targeting carnitine palmitoyl transferase 1A (CPT1A) induces ferroptosis and synergizes with immunotherapy in lung cancer.

Lei Ma, Chong Chen, Chunxing Zhao, Tong Li, Lingyu Ma, Jiayu Jiang, Zhaojun Duan, Qin Si, Tsung-Hsien Chuang, Rong Xiang and 1 more

Open access · goldAbstract read
In one paragraph

Article in Signal transduction and targeted therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 160 papers.

0numbers the graph read from it
0cells of the map it votes in
160citing papers in PubMed
61.6field-weighted citation impact, top 1% of its field
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

160 citing papers in PubMed, 147 citations in OpenAlex.

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  7. Ferroptosis in cancer: molecular mechanisms, biological roles, and therapeutic significance.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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100 more citing papers are in PubMed but not listed here.

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

11 authors at 3 institutions in 2 countries.

Lei Ma *Department of Immunology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences; School of Basic Medicine, Peking Union Medical College, Beijing, 100005, China.
Chong Chen *Department of Immunology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences; School of Basic Medicine, Peking Union Medical College, Beijing, 100005, China. chenchong86@ibms.pumc.edu.cn.ORCID 0000-0001-7191-3761
Chunxing ZhaoDepartment of Immunology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences; School of Basic Medicine, Peking Union Medical College, Beijing, 100005, China.
Tong LiDepartment of Lung Cancer Surgery, Tianjin Medical University General Hospital, Tianjin, 300052, China.
Lingyu MaDepartment of Immunology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences; School of Basic Medicine, Peking Union Medical College, Beijing, 100005, China.
Jiayu JiangDepartment of Immunology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences; School of Basic Medicine, Peking Union Medical College, Beijing, 100005, China.
Zhaojun DuanDepartment of Immunology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences; School of Basic Medicine, Peking Union Medical College, Beijing, 100005, China.
Qin SiDepartment of Immunology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences; School of Basic Medicine, Peking Union Medical College, Beijing, 100005, China.
Tsung-Hsien ChuangImmunology Research Center, National Health Research Institutes, Zhunan, Miaoli, Taiwan, ROC.
Rong XiangDepartment of Immunology, Nankai University, Tianjin, 300071, China.ORCID 0000-0003-3487-7348
Yunping LuoDepartment of Immunology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences; School of Basic Medicine, Peking Union Medical College, Beijing, 100005, China. ypluo@ibms.pumc.edu.cn.
Chinese Academy of Medical Sciences & Peking Union Medical College · CNNational Health Research Institutes · TWNankai University · CN

Funding

Ministry of Science and Technology of the People's Republic of China (Chinese Ministry of Science and Technology) 2018YFE0114300National Natural Science Foundation of China (National Science Foundation of China) 81972795National Natural Science Foundation of China (National Science Foundation of China) 82273220National Natural Science Foundation of China (National Science Foundation of China) 82373100
6 · The paper itself

Abstract

Despite the successful application of immune checkpoint therapy, no response or recurrence is typical in lung cancer. Cancer stem cells (CSCs) have been identified as a crucial player in immunotherapy-related resistance. Ferroptosis, a form of cell death driven by iron-dependent lipid peroxidation, is highly regulated by cellular metabolism remolding and has been shown to have synergistic effects when combined with immunotherapy. Metabolic adaption of CSCs drives tumor resistance, yet the mechanisms of their ferroptosis defense in tumor immune evasion remain elusive. Here, through metabolomics, transcriptomics, a lung epithelial-specific Cpt1a-knockout mouse model, and clinical analysis, we demonstrate that CPT1A, a key rate-limiting enzyme of fatty acid oxidation, acts with L-carnitine, derived from tumor-associated macrophages to drive ferroptosis-resistance and CD8

Indexed as

FerroptosisLung NeoplasmsAnimalsCarnitineCD8-Positive T-LymphocytesCell Line, TumorImmunotherapyMiceCarnitine

Identifiers

PMID38453925
PMCPMC10920667
OpenAlexW4392557146

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.