Evidence map›Paper›PMID 36959535›Full record

ArticleCellular & molecular biology letters2023

Extracellular vesicles derived from CD4

Guo-Wei Tu, Yi Zhang, Jie-Fei Ma, Jun-Yi Hou, Guang-Wei Hao, Ying Su, Jing-Chao Luo, Lulu Sheng, Zhe Luo

Erratum issuedOpen access · goldFull text read
In one paragraph

Article in Cellular & molecular biology letters, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

19 citing papers in PubMed, 23 citations in OpenAlex.

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  16. Correction: Extracellular vesicles derived from CD4Cellular & molecular biology letters · 2024
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Guo-Wei Tu *Cardiac Intensive Care Center, Zhongshan Hospital, Fudan University, Shanghai, China.
Yi Zhang *Biomedical Research Center, Institute for Clinical Sciences, Zhongshan Hospital, Fudan University, Shanghai, China.
Jie-Fei Ma *Department of Critical Care Medicine, Zhongshan Hospital (Xiamen), Fudan University, Xiamen, China.
Jun-Yi HouCardiac Intensive Care Center, Zhongshan Hospital, Fudan University, Shanghai, China.
Guang-Wei HaoCardiac Intensive Care Center, Zhongshan Hospital, Fudan University, Shanghai, China.
Ying SuCardiac Intensive Care Center, Zhongshan Hospital, Fudan University, Shanghai, China.
Jing-Chao LuoCardiac Intensive Care Center, Zhongshan Hospital, Fudan University, Shanghai, China.
Lulu ShengDepartment of Emergency Medicine, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China. yl20111211856@sjtu.edu.cn.ORCID http://orcid.org/0000-0002-5327-8933
Zhe LuoCardiac Intensive Care Center, Zhongshan Hospital, Fudan University, Shanghai, China. luo.zhe@zs-hospital.sh.cn.
Fudan University · CNShanghai Jiao Tong University · CN

Funding

National Natural Science Foundation of China 82070085
6 · The paper itself

Abstract

backgroundSepsis is an abnormal immune response after infection, wherein the lung is the most susceptible organ to fail, leading to acute lung injury. To overcome the limitations of current therapeutic strategies and develop more specific treatment, the inflammatory process, in which T cell-derived extracellular vesicles (EVs) play a central role, should be explored deeply.

methodsLiquid chromatography-tandem mass spectrometry was performed for serum EV protein profiling. The serum diacylglycerol kinase kappa (DGKK) and endotoxin contents of patients with sepsis-induced lung injury were measured. Apoptosis, oxidative stress, and inflammation in A549 cells, bronchoalveolar lavage fluid, and lung tissues of mice were measured by flow cytometry, biochemical analysis, enzyme-linked immunosorbent assay, quantitative real-time polymerase chain reaction, and western blot.

resultsDGKK, the key regulator of the diacylglycerol (DAG)/protein kinase C (PKC) pathway, exhibited elevated expression in serum EVs of patients with sepsis-induced lung injury and showed strong correlation with sepsis severity and disease progression. DGKK was expressed in CD4

conclusionsThis approach established the mechanism that T-cell-derived EVs carrying DGKK triggered alveolar epithelial cell apoptosis, oxidative stress, inflammation, and tissue damage in sepsis-induced lung injury through the DAG/PKC/NOX4 pathway. Thus, T-cell-derived EVs and the elevated distribution of DGKK should be further investigated to develop therapeutic strategies for sepsis-induced lung injury.

Indexed as

Acute Lung InjuryExtracellular VesiclesSepsisAnimalsCD4-Positive T-LymphocytesDiacylglycerol KinaseInflammationMiceOxidative StressT-LymphocytesDiacylglycerol KinaseDGKKExtracellular vesiclesInflammationOxidative stressSepsis-induced lung injury

Identifiers

PMID36959535
PMCPMC10035494
OpenAlexW4360610054

What OpenQuestion holds

Textfull text, public
LicenceCC BY
measurements read69
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.