Evidence map›Paper›PMID 36195926›Full record

ReviewJournal of neuroinflammation2022

Emerging role of STING signalling in CNS injury: inflammation, autophagy, necroptosis, ferroptosis and pyroptosis.

Xinli Hu, Haojie Zhang, Qianxin Zhang, Xue Yao, Wenfei Ni, Kailiang Zhou

Open access · goldAbstract readReview
In one paragraph

Review in Journal of neuroinflammation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 139 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
139citing papers in PubMed, 3 pooled it
17.7field-weighted citation impact, top 1% 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

139 citing papers in PubMed, 3 syntheses or guidelines pooled it, 225 citations in OpenAlex.

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  9. [Thymosin β4 inhibits pyroptosis in BV2 microglial cells: a mechanistic studyZhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2026
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79 more citing papers are in PubMed but not listed here.

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

6 authors at 3 institutions in 1 country.

Xinli Hu *Department of Orthopaedics, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, 325027, China.
Haojie Zhang *Department of Orthopaedics, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, 325027, China.
Qianxin ZhangThe First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, Zhejiang, China.
Xue YaoTianjin Key Laboratory of Spine and Spinal Cord, Department of Orthopaedics, Tianjin Medical University General Hospital, Tianjin, 300050, China.
Wenfei NiDepartment of Orthopaedics, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, 325027, China. niwenfei@126.com.
Kailiang ZhouDepartment of Orthopaedics, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, 325027, China. zhoukailiang@wmu.edu.cn.
Wenzhou Medical University · CNFirst Affiliated Hospital of Wenzhou Medical University · CNTianjin Medical University General Hospital · CN

Funding

Natural Science Foundation of Zhejiang Province LY17H060009Natural Science Foundation of Zhejiang Province Y21H060050Zhejiang Province Public Welfare Technology Application Research Project LGF20H150003
6 · The paper itself

Abstract

Stimulator of interferons genes (STING), which is crucial for the secretion of type I interferons and proinflammatory cytokines in response to cytosolic nucleic acids, plays a key role in the innate immune system. Studies have revealed the participation of the STING pathway in unregulated inflammatory processes, traumatic brain injury (TBI), spinal cord injury (SCI), subarachnoid haemorrhage (SAH) and hypoxic-ischaemic encephalopathy (HIE). STING signalling is markedly increased in CNS injury, and STING agonists might facilitate the pathogenesis of CNS injury. However, the effects of STING-regulated signalling activation in CNS injury are not well understood. Aberrant activation of STING increases inflammatory events, type I interferon responses, and cell death. cGAS is the primary pathway that induces STING activation. Herein, we provide a comprehensive review of the latest findings related to STING signalling and the cGAS-STING pathway and highlight the control mechanisms and their functions in CNS injury. Furthermore, we summarize and explore the most recent advances toward obtaining an understanding of the involvement of STING signalling in programmed cell death (autophagy, necroptosis, ferroptosis and pyroptosis) during CNS injury. We also review potential therapeutic agents that are capable of regulating the cGAS-STING signalling pathway, which facilitates our understanding of cGAS-STING signalling functions in CNS injury and the potential value of this signalling pathway as a treatment target.

Indexed as

Central Nervous System DiseasesFerroptosisInterferon Type INucleic AcidsAutophagyCytokinesHumansInflammationMembrane ProteinsNecroptosisNucleotidyltransferasesPyroptosisCytokinesInterferon Type IMembrane ProteinsNucleic AcidsNucleotidyltransferasesCell deathCentral nervous system injurycGASInflammationSTING

Identifiers

PMID36195926
PMCPMC9531511
OpenAlexW4301183068

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.