Evidence map›Paper›PMID 34445694›Full record

ReviewInternational journal of molecular sciences2021

Mitochondrial Dysfunction in Vascular Wall Cells and Its Role in Atherosclerosis.

Diana Salnikova, Varvara Orekhova, Andrey Grechko, Antonina Starodubova, Evgeny Bezsonov, Tatyana Popkova, Alexander Orekhov

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 2 pooled it
4.0field-weighted citation impact, top 5% 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

48 citing papers in PubMed, 2 syntheses or guidelines pooled it, 72 citations in OpenAlex.

  1. Pooled it
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  9. HYQTD Drug-containing Serum Alleviates HCurrent pharmaceutical biotechnology · 2026
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  18. PMCell biochemistry and biophysics · 2025
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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 5 institutions in 1 country.

Diana SalnikovaFaculty of Medicine, Lomonosov Moscow State University, 119192 Moscow, Russia.ORCID 0000-0002-0809-3710
Varvara OrekhovaLaboratory of Angiopathology, Institute of General Pathology and Pathophysiology, 125315 Moscow, Russia.
Andrey GrechkoFederal Scientific Clinical Center for Resuscitation and Rehabilitation, 109240 Moscow, Russia.
Antonina StarodubovaFederal Research Centre for Nutrition, Biotechnology and Food Safety, 109240 Moscow, Russia.
Evgeny BezsonovLaboratory of Angiopathology, Institute of General Pathology and Pathophysiology, 125315 Moscow, Russia.ORCID 0000-0002-9382-8338
Tatyana PopkovaV. A. Nasonova Institute of Rheumatology, 115522 Moscow, Russia.
Alexander OrekhovLaboratory of Angiopathology, Institute of General Pathology and Pathophysiology, 125315 Moscow, Russia.ORCID 0000-0002-3318-4681
Research Institute of General Pathology and Pathophysiology, the Russian Academy of Medical Sciences · RUAssociation of Rheumatologists of Russia · RUFederal Research Centre of Nutrition and Biotechnology · RULomonosov Moscow State University · RUV.A. Negovsky Scientific Research Institute of General Reanimatology · RU

Funding

Russian Science Foundation 18-15-00254
6 · The paper itself

Abstract

Altered mitochondrial function is currently recognized as an important factor in atherosclerosis initiation and progression. Mitochondrial dysfunction can be caused by mitochondrial DNA (mtDNA) mutations, which can be inherited or spontaneously acquired in various organs and tissues, having more or less profound effects depending on the tissue energy status. Arterial wall cells are among the most vulnerable to mitochondrial dysfunction due to their barrier and metabolic functions. In atherosclerosis, mitochondria cause alteration of cellular metabolism and respiration and are known to produce excessive amounts of reactive oxygen species (ROS) resulting in oxidative stress. These processes are involved in vascular disease and chronic inflammation associated with atherosclerosis. Currently, the list of known mtDNA mutations associated with human pathologies is growing, and many of the identified mtDNA variants are being tested as disease markers. Alleviation of oxidative stress and inflammation appears to be promising for atherosclerosis treatment. In this review, we discuss the role of mitochondrial dysfunction in atherosclerosis development, focusing on the key cell types of the arterial wall involved in the pathological processes. Accumulation of mtDNA mutations in isolated arterial wall cells, such as endothelial cells, may contribute to the development of local inflammatory process that helps explaining the focal distribution of atherosclerotic plaques on the arterial wall surface. We also discuss antioxidant and anti-inflammatory approaches that can potentially reduce the impact of mitochondrial dysfunction.

Indexed as

AntioxidantsArteriesAtherosclerosisDNA, MitochondrialEndothelial CellsHumansInflammationMitochondriaMutationOxidative StressPlaque, AtheroscleroticReactive Oxygen SpeciesAntioxidantsDNA, MitochondrialReactive Oxygen Speciesatherosclerosisinflammationmitochondrial DNAmitochondrionoxidative stress

Identifiers

PMID34445694
PMCPMC8396504
OpenAlexW3194705817

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.