Evidence map›Paper›PMID 32441055›Full record

ArticleJournal of cellular and molecular medicine2020

Extracellular vesicles enhance oxidative stress through P38/NF-kB pathway in ketamine-induced ulcerative cystitis.

Xiao Jian Xi, Jin Jiang Zeng, Yong Lu, Shao Hua Chen, Zhi Wen Jiang, Peng Jie He, Hua Mi

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

17 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Mitochondrial damage causes inflammation via cGAS-STING signaling in ketamine-induced cystitis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Crosstalk between Oxidative Stress and Exosomes.Oxidative medicine and cellular longevity · 2022
    Review
  13. Article
  14. The Biology and Function of Extracellular Vesicles in Cancer Development.Frontiers in cell and developmental biology · 2021
    Review
  15. Review
  16. Experimental and therapeutic medicine · 2020
    Article
  17. Article
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

7 authors at 2 institutions in 1 country.

Xiao Jian XiDepartment of Urology, First Affiliated Hospital of Guangxi Medical University, Nanning, China.ORCID 0000-0003-3043-6051
Jin Jiang ZengDepartment of Urology, Liuzhou Municipal Liutie Central Hospital, Liuzhou, China.
Yong LuDepartment of Urology, First Affiliated Hospital of Guangxi Medical University, Nanning, China.
Shao Hua ChenDepartment of Urology, First Affiliated Hospital of Guangxi Medical University, Nanning, China.
Zhi Wen JiangDepartment of Urology, First Affiliated Hospital of Guangxi Medical University, Nanning, China.
Peng Jie HeDepartment of Urology, First Affiliated Hospital of Guangxi Medical University, Nanning, China.
Hua MiDepartment of Urology, First Affiliated Hospital of Guangxi Medical University, Nanning, China.
Guangxi Medical University · CNLiuzhou General Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long-term abuse of ketamine causes ketamine-induced cystitis. The functional alterations of bladder epithelial cells in microenvironment during cystitis remain poorly understood. Here, we explored extracellular vesicles (EV) alteration in ketamine-induced toxicity. To simulate the high-concentration ketamine environment in vivo, we established an in vitro model of high ketamine using human uroepithelial cells (SV-HUC-1). Cell viability and proliferation were assessed to evaluate the effects of various concentrations (0, 0.25, 0.5, 1, 2, 4 and 8 mmol/L) of ketamine on SV-HUC-1 cells. The cell supernatant cultured at a concentration (0, 1, 2, 4 mmol/L) of ketamine was selected for EV extraction and identified. Subsequently, we assessed different groups (ketamine, ketamine plus EV blocker, EV, EV plus extracellular vesicles blocker) of oxidative stress and expression of inflammation. Last, luciferase reporter assay was performed to study the transcriptional regulation of EV on the NF-kB and P38 pathway. The results of our study suggested that treatment with 0, 1, 2 or 4 mmol/L ketamine altered the morphology and secretion capacity of extracellular vesicles. As the concentration of ketamine increased, the average particle size of EV decreased, but the crest size, particle concentration and EV protein increased. Moreover, after the addition of EV blocker, EV secreted at different concentrations were blocked outside the cell membrane, and the degree of oxidative stress decreased. Our study provided evidence that ketamine alters the secretion of EV by directly stimulating cells in inflammation microenvironment and EV play significant roles in intercellular signal communication and the formation of KIC.EV.

Indexed as

Oxidative StressSignal TransductionApoptosisCell Line, TumorCell SurvivalCystitisCytochalasin DExtracellular VesiclesHumansKetamineNF-kappa Bp38 Mitogen-Activated Protein KinasesUlcerCytochalasin DKetamineNF-kappa Bp38 Mitogen-Activated Protein Kinasesextracellular vesiclesketamine-induced cystitisoxidative stress

Identifiers

PMID32441055
PMCPMC7339200
OpenAlexW3028285098

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.