Evidence map›Paper›PMID 31744449›Full record

ReviewCurrent neuropharmacology2020

Mitochondrion as a Selective Target for the Treatment of Atherosclerosis: Role of Mitochondrial DNA Mutations and Defective Mitophagy in the Pathogenesis of Atherosclerosis and Chronic Inflammation.

Alexander N Orekhov, Anastasia V Poznyak, Igor A Sobenin, Nikita N Nikifirov, Ekaterina A Ivanova

Open access · greenAbstract readReview
In one paragraph

Review in Current neuropharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 2 pooled it
5.6field-weighted citation impact, top 3% 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, 2 syntheses or guidelines pooled it, 67 citations in OpenAlex.

  1. Pooled it
  2. Association Between Mitochondrial DNA Copy Number and Head and Neck Squamous Cell Carcinoma: A Systematic Review and Dose-Response Meta-Analysis.Medical science monitor : international medical journal of experimental and clinical research · 2021
    Pooled it
  3. Review
  4. From lipid overload to autophagy collapse: how lipid dysregulation drives chronic inflammation and metabolic disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
  5. Atherosclerosis: A Pathologist's Perspective.Journal of cardiovascular development and disease · 2026
    Review
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  7. Article
  8. Review
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  11. Mitophagy in Hypertensive Cardiac Hypertrophy: Mechanisms and Therapeutic Implications.Journal of clinical hypertension (Greenwich, Conn.) · 2025
    Review
  12. Article
  13. Review
  14. Article
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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

5 authors at 2 institutions in 1 country.

Alexander N OrekhovInstitute for Atherosclerosis Research, Skolkovo Innovative Center, Moscow 121609, Russian Federation
Anastasia V PoznyakInstitute for Atherosclerosis Research, Skolkovo Innovative Center, Moscow 121609, Russian Federation
Igor A SobeninInstitute for Atherosclerosis Research, Skolkovo Innovative Center, Moscow 121609, Russian Federation
Nikita N NikifirovLaboratory of Angiopathology, Institute of General Pathology and Pathophysiology, 125315 Moscow, Russian, Federation
Ekaterina A IvanovaKeyrus Biopharma, Waterloo 1410, Belgium
Institute for Atherosclerosis Research · RUResearch Institute of General Pathology and Pathophysiology, the Russian Academy of Medical Sciences · RU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAtherosclerosis is a chronic inflammatory condition that affects different arteries in the human body and often leads to severe neurological complications, such as stroke and its sequelae. Affected blood vessels develop atherosclerotic lesions in the form of focal thickening of the intimal layer, so called atherosclerotic plaques.

objectivesDespite the high priority of atherosclerosis research for global health and the numerous preclinical and clinical studies conducted, currently, there is no effective pharmacological treatment that directly impacts atherosclerotic plaques. Many knowledge gaps exist in our understanding of the mechanisms of plaque formation. In this review, we discuss the role of mitochondria in different cell types involved in atherogenesis and provide information about mtDNA mutations associated with the disease.

resultsMitochondria of blood and arterial wall cells appear to be one of the important factors in disease initiation and development. Significant experimental evidence connects oxidative stress associated with mitochondrial dysfunction and vascular disease. Moreover, mitochondrial DNA (mtDNA) deletions and mutations are being considered as potential disease markers. Further study of mtDNA damage and associated dysfunction may open new perspectives for atherosclerosis treatment.

conclusionMitochondria can be considered as important disease-modifying factors in several chronic pathologies. Deletions and mutations of mtDNA may be used as potential disease markers. Mitochondria-targeting antioxidant therapies appear to be promising for the development of treatment of atherosclerosis and other diseases associated with oxidative stress and chronic inflammation.

Indexed as

AnimalsAtherosclerosisCholesterol, LDLDNA, MitochondrialHumansInflammationMitochondriaMitophagyMuscle, Smooth, VascularMutationOxidative StressPlaque, AtheroscleroticCholesterol, LDLDNA, MitochondrialAtherosclerosisinflammationLDL metabolismmitochondrionmtDNAoxidative stress

Identifiers

PMID31744449
PMCPMC7709151
OpenAlexW2990542525

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.