Evidence map›Paper›PMID 38821518›Full record

ArticlePathogens and disease2024

Chlamydia trachomatis upregulates lncRNA CYTOR to mediate autophagy through miR-206/MAPK1 axis.

Shan Cheng, Yi Liu, Bei He, Jinrong Zhang, Yewei Yang, Xinglv Wang, Zhongyu Li

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Pathogens and disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Frontiers in cellular and infection microbiology · 2026
    Review
  2. 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

7 authors.

Shan ChengInstitute of Pathogenic Biology, School of Nursing, Hengyang Medical College, Hunan Provincial Key Laboratory for Special Pathogens Prevention and Control, University of South China, Hengyang 421001 Hunan, China.ORCID 0009-0000-4646-3439
Yi LiuInstitute of Pathogenic Biology, School of Nursing, Hengyang Medical College, Hunan Provincial Key Laboratory for Special Pathogens Prevention and Control, University of South China, Hengyang 421001 Hunan, China.
Bei HeInstitute of Pathogenic Biology, School of Nursing, Hengyang Medical College, Hunan Provincial Key Laboratory for Special Pathogens Prevention and Control, University of South China, Hengyang 421001 Hunan, China.
Jinrong ZhangInstitute of Pathogenic Biology, School of Nursing, Hengyang Medical College, Hunan Provincial Key Laboratory for Special Pathogens Prevention and Control, University of South China, Hengyang 421001 Hunan, China.
Yewei YangInstitute of Pathogenic Biology, School of Nursing, Hengyang Medical College, Hunan Provincial Key Laboratory for Special Pathogens Prevention and Control, University of South China, Hengyang 421001 Hunan, China.
Xinglv WangInstitute of Pathogenic Biology, School of Nursing, Hengyang Medical College, Hunan Provincial Key Laboratory for Special Pathogens Prevention and Control, University of South China, Hengyang 421001 Hunan, China.
Zhongyu LiInstitute of Pathogenic Biology, School of Nursing, Hengyang Medical College, Hunan Provincial Key Laboratory for Special Pathogens Prevention and Control, University of South China, Hengyang 421001 Hunan, China.

Funding

High Level Talent Program of Hunan Provincial Health Commission 20230499National Natural Science Foundation of China 82272383Scientific Research Project of Hunan Provincial Health C202304127239
6 · The paper itself

Abstract

Chlamydia trachomatis infection can be regulated by autophagy-related genes. LncRNA CYTOR has been proven to be involved in autophagy. In this research, we investigated the role of CYTOR in autophagy induced by C. trachomatis and the potential mechanisms. After C. trachomatis infection, CYTOR and MAPK1 were up-regulated and miR-206 was down-regulated, meanwhile, the autophagy-related protein Beclin1 and LC3-Ⅱ/LC3-Ⅰ ratio were increased. Interference with CYTOR or overexpression with miR-206 downregulated the autophagy-related protein Beclin1 and the number of autophagic spots LC3, decreased the protein ratio of LC3-II/LC3-I, and upregulated the expression of P62 protein. The luciferase reporter assay confirmed that CYTOR acted as a sponge for miR-206 to target MAPK1. In addition, CYTOR promoted autophagy induced by C. trachomatis infection through the MAPK1/ERK signaling pathway activation. Taken together, we have identified a novel molecular mechanism that the CYTOR/miR-206/MAPK1 axis was involved in the regulation of autophagy in C. trachomatis infection. This work provides an experimental basis for elucidating the pathogenesis of C. trachomatis for the treatment, prevention and control of related infectious diseases.

Indexed as

AutophagyChlamydia trachomatisMicroRNAsMitogen-Activated Protein Kinase 1RNA, Long NoncodingBeclin-1Chlamydia InfectionsHeLa CellsHumansUp-RegulationBeclin-1MAPK1 protein, humanMicroRNAsMitogen-Activated Protein Kinase 1RNA, Long NoncodingAutophagyChlamydia trachomatislncRNA CYTORMAPK1miR-206

Identifiers

PMID38821518
PMCPMC11210502

What OpenQuestion 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 OpenQuestion graph.