Evidence map›Paper›PMID 37971567›Full record

ArticleMolecular biology reports2023

PPAR-γ promotes the polarization of rat retinal microglia to M2 phenotype by regulating the expression of CD200-CD200R1 under hypoxia.

Yiyi Hong, Li Jiang, Fen Tang, Mingyuan Zhang, Ling Cui, Haibin Zhong, Fan Xu, Min Li, Changzheng Chen, Lifei Chen

Abstract read
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In one paragraph

Article in Molecular biology reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.6field-weighted citation impact, top 31% 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

8 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
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  5. Activation of Hippocampal ACE2 Prevents the Dysbiosis-induced Depression-like Behavior in Mice by Enhanced Neurogenesis and Neuroprotection via Mas Receptor.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025
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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

10 authors at 3 institutions in 1 country.

Yiyi Hong *Research center of Ophthalmology, Guangxi Health Commission Key Laboratory of Ophthalmology and Related Systemic Diseases Artificial Intelligence Screening Technology & Department of Ophthalmology, Guangxi Academy of Medical Sciences, The People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, 530021, China.
Li Jiang *Research center of Ophthalmology, Guangxi Health Commission Key Laboratory of Ophthalmology and Related Systemic Diseases Artificial Intelligence Screening Technology & Department of Ophthalmology, Guangxi Academy of Medical Sciences, The People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, 530021, China.
Fen TangResearch center of Ophthalmology, Guangxi Health Commission Key Laboratory of Ophthalmology and Related Systemic Diseases Artificial Intelligence Screening Technology & Department of Ophthalmology, Guangxi Academy of Medical Sciences, The People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, 530021, China.
Mingyuan ZhangLaboratory Animal Center, Guangxi Medical University, Nanning, 530021, China.
Ling CuiResearch center of Ophthalmology, Guangxi Health Commission Key Laboratory of Ophthalmology and Related Systemic Diseases Artificial Intelligence Screening Technology & Department of Ophthalmology, Guangxi Academy of Medical Sciences, The People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, 530021, China.
Haibin ZhongResearch center of Ophthalmology, Guangxi Health Commission Key Laboratory of Ophthalmology and Related Systemic Diseases Artificial Intelligence Screening Technology & Department of Ophthalmology, Guangxi Academy of Medical Sciences, The People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, 530021, China.
Fan XuResearch center of Ophthalmology, Guangxi Health Commission Key Laboratory of Ophthalmology and Related Systemic Diseases Artificial Intelligence Screening Technology & Department of Ophthalmology, Guangxi Academy of Medical Sciences, The People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, 530021, China.
Min LiResearch center of Ophthalmology, Guangxi Health Commission Key Laboratory of Ophthalmology and Related Systemic Diseases Artificial Intelligence Screening Technology & Department of Ophthalmology, Guangxi Academy of Medical Sciences, The People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, 530021, China.
Changzheng ChenEye Center, Renmin Hospital of Wuhan University, Wuhan, 430060, China. whuchenchzh@163.com.
Lifei ChenResearch center of Ophthalmology, Guangxi Health Commission Key Laboratory of Ophthalmology and Related Systemic Diseases Artificial Intelligence Screening Technology & Department of Ophthalmology, Guangxi Academy of Medical Sciences, The People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, 530021, China. 1456978397@qq.com.ORCID http://orcid.org/0000-0003-0120-3689
The People's Hospital of Guangxi Zhuang Autonomous Region · CNWuhan University · CNGuangxi Medical University · CN

Funding

Guangxi Clinical Ophthalmic Research Center AD19245193National Natural Science Foundation of China 82060179National Natural Science Foundation of China 82070982Natural Science Foundation of Guangxi Zhuang Autonomous Region 2018GXNSFAA281128
6 · The paper itself

Abstract

backgroundRecent reports suggest that peroxisome proliferator-activated receptor-γ (PPAR-γ) could promote microglial M2 polarization to inhibit inflammation. However, the specific molecular mechanisms that trigger PPAR-γ's anti-inflammatory ability in microglia are yet to be expounded. Thus, in this study, we aimed to explore the molecular mechanisms behind the anti-inflammatory effects of PPAR-γ in hypoxia-stimulated rat retinal microglial cells. METHODS AND

resultsWe used shRNA expressing lentivirus to knock down PPAR-γ and CD200 genes, and we assessed hypoxia-induced polarization markers release - M1 (iNOS, IL-1β, IL-6, and TNF-α) and M2 (Arg-1, YM1, IL-4, and IL-10) by RT-PCR. We also monitored PPAR-γ-related signals (PPAR-γ, PPAR-γ in cytoplasm or nucleus, CD200, and CD200Rs) by Western blot and RT-PCR. Our results showed that hypoxia enhanced PPAR-γ and CD200 expressions in microglial cells. Moreover, PPAR-γ agonist 15d-PGJ

conclusionOur findings demonstrated that PPAR-γ performed an anti-inflammatory function in hypoxia-stimulated microglial cells by promoting their polarization to M2 phenotype via the CD200-CD200R1 pathway.

Indexed as

MicrogliaPPAR gammaAnimalsAnti-Inflammatory AgentsHypoxiaPhenotypeRatsReceptors, ImmunologicAnti-Inflammatory AgentsCd200 protein, ratPPAR gammaReceptors, ImmunologicCD200HypoxiaMicroglial polarizationPPAR-γ

Identifiers

PMID37971567
OpenAlexW4388724228

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.