Evidence map›Paper›PMID 35453534›Full record

ReviewBiomedicines2022

Somatic Mutations of Hematopoietic Cells Are an Additional Mechanism of Body Aging, Conducive to Comorbidity and Increasing Chronification of Inflammation.

Yegor E Yegorov, Anastasia V Poznyak, Evgeny E Bezsonov, Alexander D Zhuravlev, Nikita G Nikiforov, Khava S Vishnyakova, Alexander N Orekhov

Open access · goldAbstract readReview
In one paragraph

Review in Biomedicines, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.4field-weighted citation impact, top 43% 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

3 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
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 5 institutions in 1 country.

Yegor E YegorovEngelhardt Institute of Molecular Biology, Russian Academy of Sciences, 119991 Moscow, Russia.
Anastasia V PoznyakInstitute for Atherosclerosis Research, 121609 Moscow, Russia.ORCID 0000-0002-1516-1320
Evgeny E BezsonovLaboratory of Angiopathology, Institute of General Pathology and Pathophysiology, 125315 Moscow, Russia.ORCID 0000-0002-9382-8338
Alexander D ZhuravlevLaboratory of Angiopathology, Institute of General Pathology and Pathophysiology, 125315 Moscow, Russia.
Nikita G NikiforovLaboratory of Angiopathology, Institute of General Pathology and Pathophysiology, 125315 Moscow, Russia.ORCID 0000-0002-2082-2429
Khava S VishnyakovaEngelhardt Institute of Molecular Biology, Russian Academy of Sciences, 119991 Moscow, Russia.
Alexander N OrekhovLaboratory of Angiopathology, Institute of General Pathology and Pathophysiology, 125315 Moscow, Russia.ORCID 0000-0002-3318-4681
Engelhardt Institute of Molecular Biology · RUInstitute of Gene Biology · RUInstitute for Atherosclerosis Research · RUResearch Institute of General Pathology and Pathophysiology, the Russian Academy of Medical Sciences · RUSechenov University · RU

Funding

Russian Science Foundation 20-15-00337
6 · The paper itself

Abstract

It is known that the development of foci of chronic inflammation usually accompanies body aging. In these foci, senescent cells appear with a pro-inflammatory phenotype that helps maintain inflammation. Their removal with the help of senolytics significantly improves the general condition of the body and, according to many indicators, contributes to rejuvenation. The cells of the immune system participate in the initiation, development, and resolution of inflammation. With age, the human body accumulates mutations, including the cells of the bone marrow, giving rise to the cells of the immune system. We assume that a number of such mutations formed with age can lead to the appearance of "naive" cells with an initially pro-inflammatory phenotype, the migration of which to preexisting foci of inflammation contributes not to the resolution of inflammation but its chronicity. One of such cell variants are monocytes carrying mitochondrial mutations, which may be responsible for comorbidity and deterioration in the prognosis of the course of pathologies associated with aging, such as atherosclerosis, arthritis, osteoporosis, and neurodegenerative diseases.

Indexed as

agingbone marrowCHIPchronification of inflammationinflammationmitochondriamonocytessomatic mutations

Identifiers

PMID35453534
PMCPMC9028317
OpenAlexW4220967966

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.