Evidence map›Paper›PMID 30846680›Full record

ArticleCell death & disease2019

Regulatory roles of miR-22/Redd1-mediated mitochondrial ROS and cellular autophagy in ionizing radiation-induced BMSC injury.

Zhonglong Liu, Tao Li, Fengshuo Zhu, Si'nan Deng, Xiaoguang Li, Yue He

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

31 citing papers in PubMed, 62 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. The Role of microRNA-22 in Metabolism.International journal of molecular sciences · 2025
    Review
  7. Article
  8. Article
  9. MicroRNAs as Regulators of Radiation-Induced Oxidative Stress.Current issues in molecular biology · 2024
    Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Nutritional Sensor REDD1 in Cancer and Inflammation: Friend or Foe?International journal of molecular sciences · 2022
    Review
  17. Article
  18. Article
  19. Review
  20. 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

6 authors at 2 institutions in 1 country.

Zhonglong LiuDepartment of Oral Maxillofacial & Head and Neck Oncology, Shanghai Ninth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China, 200011.
Tao LiDepartment of Orthopedics, Shanghai Ninth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China, 200011.
Fengshuo ZhuDepartment of Oral Maxillofacial & Head and Neck Oncology, Shanghai Ninth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China, 200011.
Si'nan DengDepartment of Stomatology, Central Hospital of Min-Hang District, Shanghai, China, 201109.
Xiaoguang LiDepartment of Oral Maxillofacial & Head and Neck Oncology, Shanghai Ninth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China, 200011.
Yue HeDepartment of Oral Maxillofacial & Head and Neck Oncology, Shanghai Ninth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China, 200011. eddielew@alumni.sjtu.edu.cn.
Shanghai Jiao Tong University · CNShanghai Ninth People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ionizing radiation (IR) response has been extensively investigated in BMSCs with an increasing consensus that this type of cells showed relative radiosensitivity in vitro analysis. However, the underlying mechanism of IR-induced injury of BMSCs has not been elucidated. In current study, the regulatory role of miR-22/Redd1 pathway-mediated mitochondrial reactive oxygen species (ROS) and cellular autophagy in IR-induced apoptosis of BMSCs was determined. IR facilitated the generation and accumulation of mitochondrial ROS, which promoted IR-induced apoptosis in BMSCs; meanwhile, cellular autophagy activated by IR hold a prohibitive role on the apoptosis program. The expression of miR-22 significantly increased in BMSCs after IR exposure within 24 h. Overexpression of miR-22 evidently accelerated IR-induced accumulation of mitochondrial ROS, whereas attenuated IR stimulated cellular autophagy, thus advancing cellular apoptosis. Furthermore, we verified Redd1 as a novel target for miR-22 in rat genome. Redd1 overexpression attenuated the regulatory role of miR-22 on mitochondrial ROS generation and alleviated the inhibitive role of miR-22 on cell autophagy activated by IR, thus protecting BMSCs from miR-22-mediated cell injury induced by IR exposure. These results confirmed the role of miR-22/Redd1 pathway in the regulation of IR-induced mitochondrial ROS and cellular autophagy, and subsequent cellular apoptosis.

Indexed as

3' Untranslated RegionsAnimalsApoptosisAutophagosomesAutophagyCell SurvivalHEK293 CellsHumansMaleMesenchymal Stem CellsMicroRNAsMicroscopy, Electron, TransmissionMitochondriaRadiation, IonizingRatsRats, Sprague-Dawley3' Untranslated RegionsDdit4 protein, ratMicroRNAsMIRN22 microRNA, ratReactive Oxygen SpeciesRepressor ProteinsTranscription Factors

Identifiers

PMID30846680
PMCPMC6405932
OpenAlexW2918825317

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.