Evidence map›Paper›PMID 34269814›Full record

ArticleInvestigative ophthalmology & visual science2021

Salidroside Prevents Hypoxia-Induced Human Retinal Microvascular Endothelial Cell Damage Via miR-138/ROBO4 Axis.

Xiaoling Shi, Nuo Dong, Qi Qiu, Shanhua Li, Jiaxing Zhang

Open access · goldAbstract read
In one paragraph

Article in Investigative ophthalmology & visual science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.4field-weighted citation impact, top 17% 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

11 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. The Role of miR-138 in Cardiovascular Diseases.BioMed research international · 2025
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Anti-Candidal Activity of the Parasitic PlantAntibiotics (Basel, Switzerland) · 2021
    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

5 authors at 1 institution in 1 country.

Xiaoling ShiInstitute of Brain Diseases and Cognition, Medical College of Xiamen University, Xiamen, Fujian, China.
Nuo DongAffiliated Xiamen Eye Center, Medical College of Xiamen University, Xiamen, Fujian, China.
Qi QiuInstitute of Brain Diseases and Cognition, Medical College of Xiamen University, Xiamen, Fujian, China.
Shanhua LiInstitute of Brain Diseases and Cognition, Medical College of Xiamen University, Xiamen, Fujian, China.
Jiaxing ZhangInstitute of Brain Diseases and Cognition, Medical College of Xiamen University, Xiamen, Fujian, China.
Xiamen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Purpose: Retinopathies are associated with the injury of retinal microvascular endothelial cells. Salidroside (SAL) is a medicinal supplement that has antioxidative and cytoprotective properties. We hypothesized that SAL might have a protective function in retinopathies. This research aims to explore the function and mechanism of SAL in hypoxia-induced retinal microvascular endothelial cell injury. Methods: Human retinal microvascular endothelial cells (HRMECs) injury was induced by culturing under hypoxic condition. The function of SAL on HRMECs injury was investigated using cell counting kit-8, 5-ethynyl-2'-deoxyuridine (EdU) staining, flow cytometry, Western blotting, and enzyme linked immunosorbent assay. MicroRNA (miR)-138, roundabout 4 (ROBO4), and proteins in the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathways were examined using quantitative reverse transcription polymerase chain reaction or Western blotting. The target correlation was determined by dual-luciferase reporter analysis and RNA immunoprecipitation. Results: Hypoxia resulted in proliferation inhibition, cycle arrest, apoptosis, inflammatory reaction, and oxidative stress in HRMECs. SAL attenuated hypoxia-induced HRMECs injury via increasing cell proliferation, and mitigating cycle arrest, apoptosis, inflammatory reaction, and oxidative stress. MiR-138 expression was enhanced by hypoxia, and decreased via SAL stimulation. MiR-138 upregulation reversed the influence of SAL on hypoxia-induced HRMECs injury. ROBO4 was targeted via miR-138. ROBO4 overexpression weakened the role of miR-138 in HRMECs injury. The PI3K/AKT/mTOR pathway was inactivated under hypoxic condition, and SAL increased the activation of PI3K/AKT/mTOR pathways by decreasing miR-138. Conclusions: SAL protected against hypoxia-induced HRMECs injury through regulating miR-138/ROBO4 axis, indicating the protective potential of SAL in retinopathies.

Indexed as

Gene Expression RegulationBlotting, WesternEndothelium, VascularFlow CytometryGlucosidesHumansHypoxiaMaleMicroRNAsPhenolsRetinal DiseasesRetinal VesselsGlucosidesMicroRNAsMIRN138 microRNA, humanPhenolsrhodioloside

Identifiers

PMID34269814
PMCPMC8297420
OpenAlexW3180541933

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.