Evidence map›Paper›PMID 25214718›Full record

ArticleMediators of inflammation2014

Toll-like receptor 4 in bone marrow-derived cells contributes to the progression of diabetic retinopathy.

Hui Wang, Haojun Shi, Jing Zhang, Guoliang Wang, Jinxiang Zhang, Fagang Jiang, Qing Xiao

Open access · goldAbstract read
In one paragraph

Article in Mediators of inflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.7field-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

19 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. RAGE plays key role in diabetic retinopathy: a review.Biomedical engineering online · 2023
    Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. The role of Toll-like receptors in retinal ischemic diseases.International journal of ophthalmology · 2016
    Review
  17. Review
  18. Article
  19. 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 at 3 institutions in 2 countries.

Hui WangThe Department of Medical Genetics, Tongji Medical College Affiliated with Huazhong University of Science and Technology, 13 Hangkong Road, Wuhan, Hubei 430022, China.
Haojun ShiRadiology Department, Union Hospital Affiliated with Huazhong University of Science and Technology, 1277 Jiefang Avenue, Wuhan, Hubei 430022, China.ORCID 0000-0002-2512-5403
Jing ZhangThe Department of Ophthalmology, Union Hospital Affiliated with Huazhong University of Science and Technology, 1277 Jiefang Avenue, Wuhan, Hubei 430022, China ; The Department of Ophthalmology, No. 1 Hospital of Xian City, 30 Powder Lane, South Street, Xi'an, Shanxi 710002, China.
Guoliang WangDepartment of Surgery, University of Pittsburgh Medical Center, NW607 MUH, 3459 Fifth Avenue, Pittsburgh, PA 25213, USA.
Jinxiang ZhangThe Department of Emergency Surgery, Union Hospital Affiliated with Huazhong University of Science and Technology, 1277 Jiefang Avenue, Wuhan, Hubei 430022, China.
Fagang JiangThe Department of Ophthalmology, Union Hospital Affiliated with Huazhong University of Science and Technology, 1277 Jiefang Avenue, Wuhan, Hubei 430022, China.
Qing XiaoThe Department of Ophthalmology, Union Hospital Affiliated with Huazhong University of Science and Technology, 1277 Jiefang Avenue, Wuhan, Hubei 430022, China.
Union Hospital · CNHuazhong University of Science and Technology · CNUniversity of Pittsburgh Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic retinopathy (DR) is a major microvascular complication in diabetics, and its mechanism is not fully understood. Toll-like receptor 4 (TLR4) plays a pivotal role in the maintenance of the inflammatory state during DR, and the deletion of TLR4 eventually alleviates the diabetic inflammatory state. To further elucidate the mechanism of DR, we used bone marrow transplantation to establish reciprocal chimeric animals of TLR4 mutant mice and TLR4 WT mice combined with diabetes mellitus (DM) induction by streptozotocin (STZ) treatment to identify the role of TLR4 in different cell types in the development of the proinflammatory state during DR. TLR4 mutation did not block the occurrence of high blood glucose after STZ injection compared with WT mice but did alleviate the progression of DR and alter the expression of the small vessel proliferation-related genes, vascular endothelial growth factor (VEGF), and hypoxia inducible factor-1α (HIF-1α). Grafting bone marrow-derived cells from TLR4 WT mice into TLR4 mutant mice increased the levels of TNF-α, IL-1β, and MIP-2 and increased the damage to the retina. Similarly, VEGF and HIF-1α expression were restored by the bone marrow transplantation. These findings identify an essential role for TLR4 in bone marrow-derived cells contributing to the progression of DR.

Indexed as

AnimalsBlood GlucoseBone Marrow CellsCytokinesDiabetic RetinopathyHypoxia-Inducible Factor 1, alpha SubunitMaleMiceRetinaToll-Like Receptor 4Vascular Endothelial Growth Factor ABlood GlucoseCytokinesHypoxia-Inducible Factor 1, alpha SubunitToll-Like Receptor 4Vascular Endothelial Growth Factor A

Identifiers

PMID25214718
PMCPMC4156976
OpenAlexW2008154144

What OpenQuestion holds

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Registered trials

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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.