Evidence map›Paper›PMID 33066071›Full record

ReviewBiomolecules2020

The Dichotomous Role of Inflammation in the CNS: A Mitochondrial Point of View.

Bianca Vezzani, Marianna Carinci, Simone Patergnani, Matteo P Pasquin, Annunziata Guarino, Nimra Aziz, Paolo Pinton, Michele Simonato, Carlotta Giorgi

Abstract readReview
In one paragraph

Review in Biomolecules, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

24 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Meta-analysis of HMGB1 levels in the cerebrospinal fluid and serum of patients with epilepsy.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2023
    Pooled it
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Mitochondrial dysfunction in chronic neuroinflammatory diseases (Review).International journal of molecular medicine · 2024
    Review
  9. Mitochondrial DNA and Inflammation in Alzheimer's Disease.Current issues in molecular biology · 2023
    Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Autophagy in gastrointestinal cancers.Frontiers in oncology · 2022
    Review
  18. MitoQ Is Able to Modulate Apoptosis and Inflammation.International journal of molecular sciences · 2021
    Article
  19. Review
  20. Review
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

9 authors.

Bianca VezzaniDepartment of Medical Sciences, University of Ferrara, 44121 Ferrara, Italy.ORCID 0000-0001-5869-6301
Marianna CarinciDepartment of Medical Sciences, University of Ferrara, 44121 Ferrara, Italy.ORCID 0000-0001-8106-9656
Simone PatergnaniDepartment of Medical Sciences, University of Ferrara, 44121 Ferrara, Italy.ORCID 0000-0001-7951-9267
Matteo P PasquinDepartment of Medical Sciences, University of Ferrara, 44121 Ferrara, Italy.
Annunziata GuarinoLaboratory of Technologies for Advanced Therapy (LTTA), Technopole of Ferrara, 44121 Ferrara, Italy.
Nimra AzizLaboratory of Technologies for Advanced Therapy (LTTA), Technopole of Ferrara, 44121 Ferrara, Italy.
Paolo PintonDepartment of Medical Sciences, University of Ferrara, 44121 Ferrara, Italy.
Michele SimonatoLaboratory of Technologies for Advanced Therapy (LTTA), Technopole of Ferrara, 44121 Ferrara, Italy.
Carlotta GiorgiDepartment of Medical Sciences, University of Ferrara, 44121 Ferrara, Italy.

Funding

ERC-STG 853057-InflaPMLFondazione Umberto Veronesi na
6 · The paper itself

Abstract

Innate immune response is one of our primary defenses against pathogens infection, although, if dysregulated, it represents the leading cause of chronic tissue inflammation. This dualism is even more present in the central nervous system, where neuroinflammation is both important for the activation of reparatory mechanisms and, at the same time, leads to the release of detrimental factors that induce neurons loss. Key players in modulating the neuroinflammatory response are mitochondria. Indeed, they are responsible for a variety of cell mechanisms that control tissue homeostasis, such as autophagy, apoptosis, energy production, and also inflammation. Accordingly, it is widely recognized that mitochondria exert a pivotal role in the development of neurodegenerative diseases, such as multiple sclerosis, Parkinson's and Alzheimer's diseases, as well as in acute brain damage, such in ischemic stroke and epileptic seizures. In this review, we will describe the role of mitochondria molecular signaling in regulating neuroinflammation in central nervous system (CNS) diseases, by focusing on pattern recognition receptors (PRRs) signaling, reactive oxygen species (ROS) production, and mitophagy, giving a hint on the possible therapeutic approaches targeting mitochondrial pathways involved in inflammation.

Indexed as

EncephalitisAnimalsCentral Nervous SystemHumansImmunity, InnateInflammationMitochondriaNeuroimmunomodulationSignal TransductionAlzheimer’s diseaseepilepsyischemic strokemitochondriamultiple sclerosisneurodegenerationneuroinflammationParkinson’s disease

Identifiers

PMID33066071
PMCPMC7600410

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.