Evidence map›Paper›PMID 36066650›Full record

ReviewCellular and molecular life sciences : CMLS2022

The heterogeneity of microglial activation and its epigenetic and non-coding RNA regulations in the immunopathogenesis of neurodegenerative diseases.

Chaoyi Li, Jie Ren, Mengfei Zhang, Huakun Wang, Fang Yi, Junjiao Wu, Yu Tang

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.0field-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

26 citing papers in PubMed, 38 citations in OpenAlex.

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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

7 authors at 1 institution in 2 countries.

Chaoyi LiAging Research Center, Department of Geriatrics, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Jie RenAging Research Center, Department of Geriatrics, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Mengfei ZhangAging Research Center, Department of Geriatrics, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Huakun WangAging Research Center, Department of Geriatrics, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Fang YiAging Research Center, Department of Geriatrics, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Junjiao WuNational Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Yu TangAging Research Center, Department of Geriatrics, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China. tangyusky@csu.edu.cn.ORCID http://orcid.org/0000-0001-9709-9614
Central South University · CN

Funding

Innovative Research Group Project of the National Natural Science Foundation of China 81901223National Natural Sciences Foundation of China 81801200Natural Science Foundation of Hunan Province 2019JJ40476Natural Science Foundation of Hunan Province 2022JJ40824
6 · The paper itself

Abstract

Microglia are resident immune cells in the brain and play a central role in the development and surveillance of the nervous system. Extensive gliosis is a common pathological feature of several neurodegenerative diseases, such as Alzheimer's disease (AD), the most common cause of dementia. Microglia can respond to multiple inflammatory insults and later transform into different phenotypes, such as pro- and anti-inflammatory phenotypes, thereby exerting different functions. In recent years, an increasing number of studies based on both traditional bulk sequencing and novel single-cell/nuclear sequencing and multi-omics analysis, have shown that microglial phenotypes are highly heterogeneous and dynamic, depending on the severity and stage of the disease as well as the particular inflammatory milieu. Thus, redirecting microglial activation to beneficial and neuroprotective phenotypes promises to halt the progression of neurodegenerative diseases. To this end, an increasing number of studies have focused on unraveling heterogeneous microglial phenotypes and their underlying molecular mechanisms, including those due to epigenetic and non-coding RNA modulations. In this review, we summarize the epigenetic mechanisms in the form of DNA and histone modifications, as well as the general non-coding RNA regulations that modulate microglial activation during immunopathogenesis of neurodegenerative diseases and discuss promising research approaches in the microglial era.

Indexed as

Neurodegenerative DiseasesEpigenesis, GeneticHumansMacrophage ActivationMicrogliaRNA, UntranslatedRNA, UntranslatedDNA modificationEpigenetic regulationHistone modificationMicroglial activationMicroglial phenotypesmRNA modificationNeurodegenerative diseaseNon-coding RNA

Identifiers

PMID36066650
PMCPMC11803019
OpenAlexW4294733796

What OpenQuestion holds

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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.