Evidence map›Paper›PMID 32528276›Full record

ReviewFrontiers in pharmacology2020

Cellular Mechanisms of Human Atherogenesis: Focus on Chronification of Inflammation and Mitochondrial Mutations.

Alexander M Markin, Igor A Sobenin, Andrey V Grechko, Dongwei Zhang, Alexander N Orekhov

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Frontiers in pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

24 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
  2. Considerations on the Development of Therapeutics in Vascular Calcification.Journal of cardiovascular development and disease · 2025
    Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. The Role of Adipokines in Inflammatory Mechanisms of Obesity.International journal of molecular sciences · 2022
    Review
  14. Article
  15. Atheroprotective Effects ofMolecules (Basel, Switzerland) · 2022
    Review
  16. Review
  17. Review
  18. Review
  19. Article
  20. 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

5 authors at 4 institutions in 2 countries.

Alexander M MarkinLaboratory of Infection Pathology and Molecular Microecology, Institute of Human Morphology, Moscow, Russia.
Igor A SobeninLaboratory of Medical Genetics, Institute of Experimental Cardiology, National Medical Research Center of Cardiology, Moscow, Russia.
Andrey V GrechkoFederal Research and Clinical Center of Intensive Care Medicine and Rehabilitology, Moscow, Russia.
Dongwei ZhangDiabetes Research Centre, Traditional Chinese Medicine School, Beijing University of Chinese Medicine, Beijing, China.
Alexander N OrekhovLaboratory of Infection Pathology and Molecular Microecology, Institute of Human Morphology, Moscow, Russia.
Research Institute of General Pathology and Pathophysiology, the Russian Academy of Medical Sciences · RUBeijing University of Chinese Medicine · CNResearch Institute of Human Morphology · RUV.A. Negovsky Scientific Research Institute of General Reanimatology · RU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atherosclerosis is one of the most common diseases of the cardiovascular system that leads to the development of life-threatening conditions, such as heart attack and stroke. Arthrosclerosis affects various arteries in the human body, but is especially dangerous in the arteries alimenting heart and brain, aorta, and arteries of the lower limbs. By its pathophysiology, atherosclerosis is an inflammatory disease. During the pathological process, lesions of arterial intima in the form of focal thickening are observed, which form atherosclerotic plaques as the disease progresses further. Given the significance of atherosclerosis for the global health, the search for novel effective therapies is highly prioritized. However, despite the constant progress, our understanding of the mechanisms of atherogenesis is still incomplete. One of the remaining puzzles in atherosclerosis development is the focal distribution of atherosclerotic lesions in the arterial wall. It implies the existence of certain mosaicism within the tissue, with some areas more susceptible to disease development than others, which may prove to be important for novel therapy development. There are many hypotheses explaining this phenomenon, for example, the influence of viruses, and the spread in the endothelium of the vessel multinucleated giant endothelial cells. We suggest the local variations of the mitochondrial genome as a possible explanation of this mosaicism. In this review, we discuss the role of genetic variations in the nuclear and mitochondrial genomes that influence the development of atherosclerosis. Changes in the mitochondrial and nuclear genome have been identified as independent factors for the development of the disease, as well as potential diagnostic markers.

Indexed as

atherosclerosisinflammationmitochondriamtDNAmutationsnuclear genome

Identifiers

PMID32528276
PMCPMC7247837
OpenAlexW3024502678

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.