Evidence map›Paper›PMID 31937559›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2020

Neuronal Mitochondria Modulation of LPS-Induced Neuroinflammation.

Micah Harland, Sandy Torres, Jingyi Liu, Xinglong Wang

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 1 pooled it
6.0field-weighted citation impact, top 3% 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

66 citing papers in PubMed, 1 synthesis or guideline pooled it, 119 citations in OpenAlex.

  1. Pooled it
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  17. Mitochondrial dysfunction in chronic neuroinflammatory diseases (Review).International journal of molecular medicine · 2024
    Review
  18. Charcot-Marie-Tooth type 2A in vivo models: Current updates.Journal of cellular and molecular medicine · 2024
    Review
  19. Article
  20. Review

6 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

4 authors at 1 institution in 1 country.

Micah HarlandDepartment of Pathology, and.
Sandy TorresDepartment of Pathology, and.
Jingyi LiuDepartment of Pathology, and.
Xinglong WangDepartment of Pathology, and xinglong.wang@case.edu.
Case Western Reserve University · US

Funding

Immunology Training Program-PredoctoralT32AI089474 · NIAID · CASE WESTERN RESERVE UNIVERSITY · PI COBB, BRIAN A · 2010 to 2025
$3.4M
Mitochondrial dynamics for the maintenance of neuromuscular junctions during aging and in ALSR01NS097679 · NINDS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI WANG, XINGLONG · 2017 to 2021
$2.0M
Mitochondrial TDP-43 in Alzheimer's DiseaseRF1AG056320 · NIA · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI WANG, XINGLONG · 2019 to 2019
$2.0M
NIAID NIH HHS T32 AI089474NIA NIH HHS RF1 AG056320NINDS NIH HHS R01 NS097679
6 · The paper itself

Abstract

Neuronal mitochondria dysfunction and neuroinflammation are two prominent pathological features increasingly realized as important pathogenic mechanisms for neurodegenerative diseases. However, little attempt has been taken to investigate the likely interactions between them. Mitofusin2 (Mfn2) is a mitochondrial outer membrane protein regulating mitochondrial fusion, a dynamic process essential for mitochondrial function. To explore the significance of neuronal mitochondria in the regulation of neuroinflammation, male and female transgenic mice with forced overexpression of Mfn2 specifically in neurons were intraperitoneally injected with lipopolysaccharide (LPS), a widely used approach to model neurodegeneration-associated neuroinflammation. Remarkably, LPS-induced lethality was almost completely abrogated in neuronal Mfn2 overexpression mice. Compared with nontransgenic wild-type mice, mice with neuronal Mfn2 overexpression also exhibited alleviated bodyweight loss, behavioral sickness, and myocardial dysfunction. LPS-induced release of IL-1β but not TNF-α was further found greatly inhibited in the CNS of mice with neuronal Mfn2 overexpression, whereas peripheral inflammatory responses in the blood, heart, lung, and spleen remained unchanged. At the cellular and molecular levels, neuronal Mfn2 suppressed the activation of microglia, prevented LPS-induced mitochondrial fragmentation in neurons, and importantly, upregulated the expression of CX3CL1, a unique chemokine constitutively produced by neurons to suppress microglial activation. Together, these results reveal an unrecognized possible role of neuronal mitochondria in the regulation of microglial activation, and propose neuronal Mfn2 as a likely mechanistic linker between neuronal mitochondria dysfunction and neuroinflammation in neurodegeneration.

Indexed as

AnimalsFemaleGTP PhosphohydrolasesInflammationLipopolysaccharidesMaleMiceMice, TransgenicMicrogliaMitochondriaNeuronsGTP PhosphohydrolasesLipopolysaccharidesMfn2 protein, mouseLPSMfn2mitochondrial dynamicsneuroinflammationsepsisseptic myocardial dysfunction

Identifiers

PMID31937559
PMCPMC7046320
OpenAlexW2999706510

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.