Evidence map›Paper›PMID 33672477›Full record

ReviewBiomedicines2021

Mitochondrial Oxidative Stress and "Mito-Inflammation": Actors in the Diseases.

Simone Patergnani, Esmaa Bouhamida, Sara Leo, Paolo Pinton, Alessandro Rimessi

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 108 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
108citing papers in PubMed, 1 pooled it
8.4field-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

108 citing papers in PubMed, 1 synthesis or guideline pooled it, 146 citations in OpenAlex.

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  12. Roles of the Altitude-Adapted Immune Microenvironment in Pulmonary Vascular Remodeling in High-Altitude Pulmonary Hypertension: A Review.Medical science monitor : international medical journal of experimental and clinical research · 2026
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48 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

5 authors at 1 institution in 1 country.

Simone PatergnaniDepartment of Medical Sciences and Laboratory for Technologies of Advanced Therapies (LTTA), University of Ferrara, 44121 Ferrara, Italy.ORCID 0000-0001-7951-9267
Esmaa BouhamidaDepartment of Medical Sciences and Laboratory for Technologies of Advanced Therapies (LTTA), University of Ferrara, 44121 Ferrara, Italy.
Sara LeoDepartment of Medical Sciences and Laboratory for Technologies of Advanced Therapies (LTTA), University of Ferrara, 44121 Ferrara, Italy.
Paolo PintonDepartment of Medical Sciences and Laboratory for Technologies of Advanced Therapies (LTTA), University of Ferrara, 44121 Ferrara, Italy.ORCID 0000-0001-7108-6508
Alessandro RimessiDepartment of Medical Sciences and Laboratory for Technologies of Advanced Therapies (LTTA), University of Ferrara, 44121 Ferrara, Italy.ORCID 0000-0001-7091-5765
University of Ferrara · IT

Funding

Associazione Italiana per la Ricerca sul Cancro IG-23670Fondazione per la Ricerca sulla Fibrosi Cistica 19/2014Fondazione per la Ricerca sulla Fibrosi Cistica FFC#12/2010Fondazione per la Ricerca sulla Fibrosi Cistica FFC #20/2015Fondazione Telethon GGP11139BItalian Ministry of Education, University and Research PRIN Grant 2017E5L5P3Italian Ministry of Education, University and Research PRIN Grant 2017XA5J5NItalian Ministry of Health GR-2016-02364602Università degli Studi di Ferrara FIR-2017
6 · The paper itself

Abstract

A decline in mitochondrial redox homeostasis has been associated with the development of a wide range of inflammatory-related diseases. Continue discoveries demonstrate that mitochondria are pivotal elements to trigger inflammation and stimulate innate immune signaling cascades to intensify the inflammatory response at front of different stimuli. Here, we review the evidence that an exacerbation in the levels of mitochondrial-derived reactive oxygen species (ROS) contribute to mito-inflammation, a new concept that identifies the compartmentalization of the inflammatory process, in which the mitochondrion acts as central regulator, checkpoint, and arbitrator. In particular, we discuss how ROS contribute to specific aspects of mito-inflammation in different inflammatory-related diseases, such as neurodegenerative disorders, cancer, pulmonary diseases, diabetes, and cardiovascular diseases. Taken together, these observations indicate that mitochondrial ROS influence and regulate a number of key aspects of mito-inflammation and that strategies directed to reduce or neutralize mitochondrial ROS levels might have broad beneficial effects on inflammatory-related diseases.

Indexed as

cancerdiabetesgastrointestinal disordersmitochondriamito-inflammationneurodegenerative disordersoxidative stresspulmonary diseases

Identifiers

PMID33672477
PMCPMC7923430
OpenAlexW3130968559

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.