Evidence map›Paper›PMID 33317392›Full record

ArticleAutophagy2021

PARP14 inhibits microglial activation via LPAR5 to promote post-stroke functional recovery.

Ying Tang, Jinchang Liu, Yu Wang, Li Yang, Bing Han, Yuan Zhang, Ying Bai, Ling Shen, Mingyue Li, Teng Jiang and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in Autophagy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.5field-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

36 citing papers in PubMed, 66 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

16 authors at 3 institutions in 1 country.

Ying TangDepartment of Pharmacology, School of Medicine, Southeast University, Nanjing, Jiangsu, China.
Jinchang LiuJiangsu Key Laboratory of Drug Design and Optimization, Department of Medicinal Chemistry, China Pharmaceutical University, Nanjing, China.
Yu WangDepartment of Pharmacology, School of Medicine, Southeast University, Nanjing, Jiangsu, China.
Li YangDepartment of Pharmacology, School of Medicine, Southeast University, Nanjing, Jiangsu, China.
Bing HanDepartment of Pharmacology, School of Medicine, Southeast University, Nanjing, Jiangsu, China.
Yuan ZhangDepartment of Pharmacology, School of Medicine, Southeast University, Nanjing, Jiangsu, China.
Ying BaiDepartment of Pharmacology, School of Medicine, Southeast University, Nanjing, Jiangsu, China.
Ling ShenDepartment of Pharmacology, School of Medicine, Southeast University, Nanjing, Jiangsu, China.
Mingyue LiDepartment of Pharmacology, School of Medicine, Southeast University, Nanjing, Jiangsu, China.
Teng JiangJiangsu Key Laboratory of Drug Design and Optimization, Department of Medicinal Chemistry, China Pharmaceutical University, Nanjing, China.
Qingqing YeDepartment of Pharmacology, School of Medicine, Southeast University, Nanjing, Jiangsu, China.
Xiaoyu YuDepartment of Pharmacology, School of Medicine, Southeast University, Nanjing, Jiangsu, China.
Rongrong HuangDepartment of Pharmacology, School of Medicine, Southeast University, Nanjing, Jiangsu, China.
Zhao ZhangState Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Materia Medica & Neuroscience Center, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Yungen XuJiangsu Key Laboratory of Drug Design and Optimization, Department of Medicinal Chemistry, China Pharmaceutical University, Nanjing, China.
Honghong YaoDepartment of Pharmacology, School of Medicine, Southeast University, Nanjing, Jiangsu, China.
Southeast University · CNChina Pharmaceutical University · CNChinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Stroke is a major public health problem leading to high rates of death and disability worldwide, but no effective pharmacological therapy is currently available except for the use of PLAT (plasminogen activator, tissue). Here we show that PARP14 (poly (ADP-ribose) polymerase family, member 14) level was significantly increased in the peri-infarct zone of photothrombotic stroke (PT) mice. Genetic knockdown and pharmacological inhibition of PARP14 aggravated functional impairment and increased infarct volume in PT mice, while overexpression of PARP14 displayed the opposite effects. Furthermore, PARP14 was abundant in microglia, and downregulation of PARP14 increased post-stroke microglial activation, whereas overexpression of PARP14 alleviated microglial activation, possibly through microglial macroautophagy/autophagy modulation. Mechanistically, overexpression of PARP14 suppressed

Indexed as

Caenorhabditis elegans ProteinsStrokeAnimalsAutophagyCaenorhabditis elegansDown-RegulationMiceMicrogliaPoly(ADP-ribose) PolymerasesRNA-Binding ProteinsCaenorhabditis elegans ProteinsFOX-1 protein, C elegansParp14 protein, mousePoly(ADP-ribose) PolymerasesRNA-Binding ProteinsAutophagyfunctional recoveryischemic strokelysophosphatidic acid receptor 5microglial activationpoly (ADP-ribose) polymerase 14

Identifiers

PMID33317392
PMCPMC8525999
OpenAlexW3111124331

What OpenQuestion holds

Textmetadata
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.