Evidence map›Paper›PMID 33572080›Full record

ReviewBiomedicines2021

Different Roles of Mitochondria in Cell Death and Inflammation: Focusing on Mitochondrial Quality Control in Ischemic Stroke and Reperfusion.

Marianna Carinci, Bianca Vezzani, Simone Patergnani, Peter Ludewig, Katrin Lessmann, Tim Magnus, Ilaria Casetta, Maura Pugliatti, Paolo Pinton, Carlotta Giorgi

Open access · goldAbstract readReview
In one paragraph

Review in Biomedicines, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 1 pooled it
4.7field-weighted citation impact, top 4% 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

46 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 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

10 authors at 2 institutions in 2 countries.

Marianna CarinciLaboratory for Technologies of Advanced Therapies, Department of Medical Sciences, University of Ferrara, 44121 Ferrara, Italy.
Bianca VezzaniLaboratory for Technologies of Advanced Therapies, Department of Medical Sciences, University of Ferrara, 44121 Ferrara, Italy.
Simone PatergnaniLaboratory for Technologies of Advanced Therapies, Department of Medical Sciences, University of Ferrara, 44121 Ferrara, Italy.ORCID 0000-0001-7951-9267
Peter LudewigDepartment of Neurology, University Medical Center Hamburg-Eppendorf, Martinistraße 52, 20251 Hamburg, Germany.
Katrin LessmannDepartment of Neurology, University Medical Center Hamburg-Eppendorf, Martinistraße 52, 20251 Hamburg, Germany.ORCID 0000-0002-6723-9265
Tim MagnusDepartment of Neurology, University Medical Center Hamburg-Eppendorf, Martinistraße 52, 20251 Hamburg, Germany.
Ilaria CasettaDepartment of Neuroscience and Rehabilitation, University of Ferrara, 44121 Ferrara, Italy.
Maura PugliattiDepartment of Neuroscience and Rehabilitation, University of Ferrara, 44121 Ferrara, Italy.
Paolo PintonLaboratory for Technologies of Advanced Therapies, Department of Medical Sciences, University of Ferrara, 44121 Ferrara, Italy.ORCID 0000-0001-7108-6508
Carlotta GiorgiLaboratory for Technologies of Advanced Therapies, Department of Medical Sciences, University of Ferrara, 44121 Ferrara, Italy.
University of Ferrara · ITUniversität Hamburg · DE

Funding

Associazione Italiana per la Ricerca sul Cancro IG-19803Associazione Italiana per la Ricerca sul Cancro IG-23670Bundesministerium für Bildung und Forschung 13XP5060BEuropean Research Council 853057-InflaPMLFondazione Umberto Veronesi Grant research Fellowship 2020German Research Foundation (DFG FOR 2879) LU 1924/1-1German Research Foundation (DFG FOR 2879) MA 4375/6-1Italian Ministry of Health GR-2013-02356747Progetti di Rilevante Interesse Nazionale PRIN20177E9EPYProgetti di Rilevante Interesse Nazionale PRIN2017E5L5P3
6 · The paper itself

Abstract

Mitochondrial dysfunctions are among the main hallmarks of several brain diseases, including ischemic stroke. An insufficient supply of oxygen and glucose in brain cells, primarily neurons, triggers a cascade of events in which mitochondria are the leading characters. Mitochondrial calcium overload, reactive oxygen species (ROS) overproduction, mitochondrial permeability transition pore (mPTP) opening, and damage-associated molecular pattern (DAMP) release place mitochondria in the center of an intricate series of chance interactions. Depending on the degree to which mitochondria are affected, they promote different pathways, ranging from inflammatory response pathways to cell death pathways. In this review, we will explore the principal mitochondrial molecular mechanisms compromised during ischemic and reperfusion injury, and we will delineate potential neuroprotective strategies targeting mitochondrial dysfunction and mitochondrial homeostasis.

Indexed as

cell deathinflammationischemic reperfusionischemic strokemitochondrial fissionmitochondrial fusionmitochondrial transfermitophagy

Identifiers

PMID33572080
PMCPMC7914955
OpenAlexW3127262694

What Socratic 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 Socratic graph.