Evidence map›Paper›PMID 38336763›Full record

ArticleStem cell research & therapy2024

NOD1 deficiency ameliorates the progression of diabetic retinopathy by modulating bone marrow-retina crosstalk.

Jingwen Qiu, Jing Wu, Wenwen Chen, Yu Ruan, Jingning Mao, Shue Li, Xuan Tang, Lei Zhao, Shengbing Li, Ke Li and 2 more

Open access · goldAbstract read
In one paragraph

Article in Stem cell research & therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

7 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Glaucomatous retinal ganglion cells: death and protection.International journal of ophthalmology · 2025
    Review
  7. 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

12 authors at 3 institutions in 1 country.

Jingwen Qiu *Department of Endocrinology and Metabolism, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Jing Wu *Department of Hematology/Oncology, Chongqing University Cancer Hospital, Chongqing, China.
Wenwen Chen *Department of Endocrinology and Metabolism, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Yu RuanDivision of Growth, Development and Mental Health of Children and Adolescence, Children's Hospital of Chongqing Medical University, Chongqing, China.
Jingning MaoHealth Medical Center, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Shue LiDepartment of Laboratory Medicine, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Xuan TangDepartment of Endocrinology and Metabolism, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Lei ZhaoCenter for Lipid Research, Key Laboratory of Molecular Biology for Infectious Diseases, Ministry of Education, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Shengbing LiDepartment of Endocrinology and Metabolism, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Ke LiDepartment of Endocrinology and Metabolism, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Dongfang LiuDepartment of Endocrinology and Metabolism, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Yaqian DuanDepartment of Endocrinology and Metabolism, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China. duanyaqian@cqmu.edu.cn.ORCID 0000-0001-5228-8606
Dalian Medical University · CNChildren's Hospital of Chongqing Medical University · CNChongqing University · CN

Funding

National Natural Science Foundation of China No. 81900758Natural Science Foundation Project of Chongqing, Chongqing Science and Technology Commission cstc2021jcyj-msxmX0250
6 · The paper itself

Abstract

backgroundNucleotide-binding oligomerization domain-containing protein 1 (NOD1) plays a pivotal role in inducing metabolic inflammation in diabetes. Additionally, the NOD1 ligand disrupts the equilibrium of bone marrow-derived hematopoietic stem/progenitor cells, a process that has immense significance in the development of diabetic retinopathy (DR). We hypothesized that NOD1 depletion impedes the advancement of DR by resolving bone marrow dysfunction.

methodsWe generated NOD1

resultsElevated circulating NOD1 activators were observed in Akita mice after 6 months of diabetes. NOD1 depletion partially restored diabetes-induced structural changes and retinal electrical responses in NOD1

conclusionsThe results of our study unveil, for the first time, the critical role of NOD1 as a trigger for a hematopoietic imbalance toward myelopoiesis and local retinal inflammation, culminating in DR progression. Targeting NOD1 in bone marrow may be a potential strategy for the prevention and treatment of DR.

Indexed as

Diabetes MellitusDiabetic RetinopathyNod1 Signaling Adaptor ProteinRetinal DegenerationAnimalsBone MarrowHematopoietic Stem CellsInflammationMiceMice, Inbred C57BLRetinaNod1 protein, mouseNod1 Signaling Adaptor ProteinDiabetic retinopathyHematopoietic stem/progenitor cellsInflammationMacrophageNucleotide-binding oligomerization domain-containing protein 1

Identifiers

PMID38336763
PMCPMC10858517
OpenAlexW4391678921

What OpenQuestion holds

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LicenceCC BY
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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.