Evidence map›Paper›PMID 33433724›Full record

ArticleCellular and molecular neurobiology2022

Sarm1 is Essential for Anesthesia-Induced Neuroinflammation and Cognitive Impairment in Aged Mice.

Huimei Lin, Zhenming Kang, Shunyuan Li, Jingyang Zeng, Jie Zhao

Open access · greenAbstract read
In one paragraph

Article in Cellular and molecular neurobiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 19% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. SARM1 can be a potential therapeutic target for spinal cord injury.Cellular and molecular life sciences : CMLS · 2022
    Review
  10. Review
  11. 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

5 authors at 1 institution in 1 country.

Huimei LinDepartment of Anesthesiology, Quanzhou First Hospital Affiliated to Fujian Medical University, Quanzhou, 362000, Fujian, China.ORCID http://orcid.org/0000-0002-8041-2384
Zhenming KangDepartment of Anesthesiology, Quanzhou First Hospital Affiliated to Fujian Medical University, Quanzhou, 362000, Fujian, China.ORCID http://orcid.org/0000-0002-1162-5984
Shunyuan LiDepartment of Anesthesiology, Quanzhou First Hospital Affiliated to Fujian Medical University, Quanzhou, 362000, Fujian, China.ORCID http://orcid.org/0000-0001-5508-2603
Jingyang ZengDepartment of Anesthesiology, Quanzhou First Hospital Affiliated to Fujian Medical University, Quanzhou, 362000, Fujian, China.ORCID http://orcid.org/0000-0003-0033-7394
Jie ZhaoDepartment of Anesthesiology, Quanzhou First Hospital Affiliated to Fujian Medical University, Quanzhou, 362000, Fujian, China. shmg1034031635@163.com.ORCID http://orcid.org/0000-0002-1497-571X
Fujian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Postoperative cognitive dysfunction (POCD) is a common phenomenon among elderly patients with unclear etiology. Sterile alpha and TIR motif-containing 1 (Sarm1) plays important roles in neuroinflammation and cognitive function, and activates Calpain which has been shown to promote POCD through TrkB cleavage. This study aims to test the hypothesis that Sarm1 is involved in POCD through regulating Calpain activity. Wild type and Sarm1 knock out mice were exposed to isoflurane. Mouse cognitive function was determined by Morris water maze test. Neuroinflammation was determined by Iba1 and GFAP protein levels and mRNA expression of proinflammatory cytokines. Calpain activation was determined by αII-spectrin degradation and TrkB cleavage. Mitogen-activated protein kinase (MAPK) signaling was determined by c-Jun N-terminal kinase and cJun phosphorylation both in vivo and in vitro by Western blot and immunofluorescence staining. We found that Sarm1 deletion suppressed isoflurane induced cognitive impairment and neuroinflammation. Deletion of Sarm1 inhibited isoflurane induced αII-spectrin degradation and TrkB cleavage, which indicates suppression of Calpain activation. Finally, deletion of Sarm1 suppressed isoflurane induced MAPK signaling both in vivo and in vitro. Our findings suggest that isoflurane anesthesia induced cognitive impairment is prevented by Sarm1 deletion in mice, making Sarm1 a potent therapeutic target for treating or preventing POCD.

Indexed as

AnesthesiaCognitive DysfunctionIsofluranePostoperative Cognitive ComplicationsAgedAnimalsArmadillo Domain ProteinsCalpainCytoskeletal ProteinsHumansMiceNeuroinflammatory DiseasesSpectrinArmadillo Domain ProteinsCalpainCytoskeletal ProteinsIsofluraneSARM1 protein, humanSARM1 protein, mouseSpectrinAnesthesiaCalpainNeuroinflammationPostoperative cognitive dysfunctionSarm1

Identifiers

PMID33433724
PMCPMC11421738
OpenAlexW3120373827

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.