Evidence map›Paper›PMID 36013333›Full record

ArticleLife (Basel, Switzerland)2022

The Role of Mitochondrial Mutations in Chronification of Inflammation: Hypothesis and Overview of Own Data.

Alexander N Orekhov, Nikita G Nikiforov, Andrey V Omelchenko, Vasily V Sinyov, Igor A Sobenin, Andrey Y Vinokurov, Varvara A Orekhova

Open access · goldAbstract read
In one paragraph

Article in Life (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.4field-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

13 citing papers in PubMed, 18 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

7 authors at 4 institutions in 1 country.

Alexander N OrekhovInstitute for Atherosclerosis Research, Osennyaya Street 4-1-207, 121609 Moscow, Russia.ORCID 0000-0002-3318-4681
Nikita G NikiforovLaboratory of Angiopathology, The Institute of General Pathology and Pathophysiology, 8 Baltiyskaya Street, 125315 Moscow, Russia.ORCID 0000-0002-2082-2429
Andrey V OmelchenkoLaboratory of Angiopathology, The Institute of General Pathology and Pathophysiology, 8 Baltiyskaya Street, 125315 Moscow, Russia.ORCID 0000-0003-4512-4413
Vasily V SinyovLaboratory of Medical Genetics, Institute of Experimental Cardiology, National Medical Research Center of Cardiology, 121552 Moscow, Russia.
Igor A SobeninLaboratory of Medical Genetics, Institute of Experimental Cardiology, National Medical Research Center of Cardiology, 121552 Moscow, Russia.ORCID 0000-0003-0978-6444
Andrey Y VinokurovCell Physiology & Pathology Laboratory of R&D Center of Biomedical Photonics, Orel State University, 95 Komsomolskaya Street, 302026 Orel, Russia.
Varvara A OrekhovaLaboratory of Angiopathology, The Institute of General Pathology and Pathophysiology, 8 Baltiyskaya Street, 125315 Moscow, Russia.
Research Institute of General Pathology and Pathophysiology, the Russian Academy of Medical Sciences · RUInstitute of Experimental Cardiology · RUInstitute for Atherosclerosis Research · RUOrel State University named after I.S. Turgenev · RU

Funding

Russian Science Foundation 22-15-00317
6 · The paper itself

Abstract

Chronic human diseases, especially age-related disorders, are often associated with chronic inflammation. It is currently not entirely clear what factors are responsible for the sterile inflammatory process becoming chronic in affected tissues. This process implies impairment of the normal resolution of the inflammatory response, when pro-inflammatory cytokine production ceases and tissue repair process begins. The important role of the mitochondria in the correct functioning of innate immune cells is currently well recognized, with mitochondrial signals being an important component of the inflammatory response regulation. In this work, we propose a hypothesis according to which mitochondrial DNA (mtDNA) mutations may play a key role in rendering certain cells prone to prolonged pro-inflammatory activation, therefore contributing to chronification of inflammation. The affected cells become sites of constant pro-inflammatory stimulation. The study of the distribution of atherosclerotic lesions on the surface of the arterial wall samples obtained from deceased patients revealed a focal distribution of lesions corresponding to the distribution of cells with altered morphology that are affected by mtDNA mutations. These observations support the proposed hypothesis and encourage further studies.

Indexed as

atherosclerosisinflammationmitophagymtDNA mutation

Identifiers

PMID36013333
PMCPMC9410061
OpenAlexW4289176764

What OpenQuestion holds

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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.