Evidence map›Paper›PMID 30903531›Full record

ArticleMolecular neurobiology2019

Rapamycin Removes Damaged Mitochondria and Protects Human Trabecular Meshwork (TM-1) Cells from Chronic Oxidative Stress.

Jing Na He, Shao Dan Zhang, Yang Qu, Hai Lin Wang, Clement C Tham, Chi Pui Pang, Wai Kit Chu

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

23 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
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  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Autophagy in Human Retinal Neurons in Glaucoma.Bulletin of experimental biology and medicine · 2022
    Article
  13. Review
  14. Review
  15. Review
  16. Review
  17. Autophagy in the Aging and Experimental Ocular Hypertensive Mouse Model.Investigative ophthalmology & visual science · 2020
    Article
  18. Review
  19. The Role of Autophagy in Glaucomatous Optic Neuropathy.Frontiers in cell and developmental biology · 2020
    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

7 authors at 3 institutions in 2 countries.

Jing Na HeDepartment of Ophthalmology and Visual Sciences, Hong Kong Eye Hospital, The Chinese University of Hong Kong, 147K Argyle Street, Kowloon, Hong Kong.
Shao Dan ZhangThe Eye Hospital, School of Ophthalmology and Optometry, Wenzhou Medical University, Zhejiang, China.
Yang QuDepartment of Ophthalmology, The Fourth People's Hospital of Shenyang, Key Laboratory of Ophthalmology of Shenyang, Shenyang Eye Research Institute, Shenyang, China.
Hai Lin WangDepartment of Ophthalmology, The Fourth People's Hospital of Shenyang, Key Laboratory of Ophthalmology of Shenyang, Shenyang Eye Research Institute, Shenyang, China.
Clement C ThamDepartment of Ophthalmology and Visual Sciences, Hong Kong Eye Hospital, The Chinese University of Hong Kong, 147K Argyle Street, Kowloon, Hong Kong.
Chi Pui PangDepartment of Ophthalmology and Visual Sciences, Hong Kong Eye Hospital, The Chinese University of Hong Kong, 147K Argyle Street, Kowloon, Hong Kong.
Wai Kit ChuDepartment of Ophthalmology and Visual Sciences, Hong Kong Eye Hospital, The Chinese University of Hong Kong, 147K Argyle Street, Kowloon, Hong Kong. waikit@cuhk.edu.hk.ORCID http://orcid.org/0000-0003-2903-3247
Chinese University of Hong Kong · HKThe Fourth People's Hospital · CNWenzhou Medical University · CN

Funding

National Natural Science Foundation of China 81100661Natural Science Foundation of Liaoning Province 2015020560
6 · The paper itself

Abstract

Glaucoma is a chronic optic neuropathy that could lead to permanent vision loss. Primary open-angle glaucoma (POAG) is the most common type of glaucoma, with elevated intraocular pressure (IOP) as a major risk factor. IOP is mainly regulated by trabecular meshwork (TM), an important component of the conventional aqueous humor (AH) outflow pathway. TM cells are constantly subjected to oxidative stress. Long-term exposure to oxidative stress has been shown to cause elevation of AH outflow resistance, leading to higher IOP. In this study, we induced chronic oxidative stress in human trabecular meshwork (TM-1) cells with 1 μM rotenone and investigated the levels of reactive oxygen species (ROS), autophagy, and mitochondrial functions. Protective effects of rapamycin, an inducer of autophagy, were also investigated. Our data indicated that rotenone significantly increased oxidative stress, but not autophagy, in TM-1 cells. Rapamycin at 10 nM effectively suppressed the rotenone-induced cell apoptosis, as well as the ROS elevation. The protective effects of rapamycin could be associated to the induction of autophagy and removal of damaged mitochondria in TM-1 cells. Our results suggest autophagy has important roles in protecting TM-1 cells from oxidative stress, which could be further developed into a novel treatment to POAG.

Indexed as

ApoptosisAutophagyCell LineCytoprotectionCytoskeletal ProteinsDexamethasoneEye ProteinsGlycoproteinsHumansMitochondriaMyocilinOxidative StressRotenoneSirolimusTrabecular MeshworkUp-RegulationCytoskeletal ProteinsDexamethasoneEye ProteinsGlycoproteinsMyocilinRotenoneSirolimusAutophagyOxidative stressPOAGTrabecular meshwork

Identifiers

PMID30903531
OpenAlexW2923251912

What OpenQuestion holds

Textmetadata
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.