Evidence map›Paper›PMID 33672784›Full record

ReviewLife (Basel, Switzerland)2021

Disturbance of Mitochondrial Dynamics and Mitochondrial Therapies in Atherosclerosis.

Alexander M Markin, Viktoria A Khotina, Xenia G Zabudskaya, Anastasia I Bogatyreva, Antonina V Starodubova, Ekaterina Ivanova, Nikita G Nikiforov, Alexander N Orekhov

Open access · goldAbstract readReview
In one paragraph

Review in Life (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

20 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
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  12. Target and Cell Therapy for Atherosclerosis and CVD.International journal of molecular sciences · 2023
    Review
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  15. Lycopene in the Prevention of Cardiovascular Diseases.International journal of molecular sciences · 2022
    Review
  16. 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

8 authors at 6 institutions in 1 country.

Alexander M MarkinLaboratory of Cellular and Molecular Pathology of Cardiovascular System, Institute of Human Morphology, 117418 Moscow, Russia.ORCID 0000-0002-6649-7924
Viktoria A KhotinaLaboratory of Cellular and Molecular Pathology of Cardiovascular System, Institute of Human Morphology, 117418 Moscow, Russia.ORCID 0000-0003-2096-3237
Xenia G ZabudskayaFSBI National Medical Research Center of Oncology named after N.N. Blokhin of the Ministry of Health of Russia, 115478 Moscow, Russia.ORCID 0000-0003-1290-574X
Anastasia I BogatyrevaLaboratory of Cellular and Molecular Pathology of Cardiovascular System, Institute of Human Morphology, 117418 Moscow, Russia.
Antonina V StarodubovaFederal Research Centre for Nutrition, Biotechnology and Food Safety, Ustinsky Passage, 109240 Moscow, Russia.
Ekaterina IvanovaDepartment of Basic Research, Institute of Atherosclerosis Research, 121609 Moscow, Russia.ORCID 0000-0003-3159-2881
Nikita G NikiforovLaboratory of Cellular and Molecular Pathology of Cardiovascular System, Institute of Human Morphology, 117418 Moscow, Russia.
Alexander N OrekhovLaboratory of Cellular and Molecular Pathology of Cardiovascular System, Institute of Human Morphology, 117418 Moscow, Russia.ORCID 0000-0002-3318-4681
Research Institute of General Pathology and Pathophysiology, the Russian Academy of Medical Sciences · RUResearch Institute of Human Morphology · RUFederal Research Centre of Nutrition and Biotechnology · RUInstitute for Atherosclerosis Research · RUInstitute of Experimental Cardiology · RUMinistry of Health of the Russian Federation · RU

Funding

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

Abstract

Mitochondrial dysfunction is associated with a wide range of chronic human disorders, including atherosclerosis and diabetes mellitus. Mitochondria are dynamic organelles that undergo constant turnover in living cells. Through the processes of mitochondrial fission and fusion, a functional population of mitochondria is maintained, that responds to the energy needs of the cell. Damaged or excessive mitochondria are degraded by mitophagy, a specialized type of autophagy. These processes are orchestrated by a number of proteins and genes, and are tightly regulated. When one or several of these processes are affected, it can lead to the accumulation of dysfunctional mitochondria, deficient energy production, increased oxidative stress and cell death-features that are described in many human disorders. While severe mitochondrial dysfunction is known to cause specific and mitochondrial disorders in humans, progressing damage of the mitochondria is also observed in a wide range of other chronic diseases, including cancer and atherosclerosis, and appears to play an important role in disease development. Therefore, correction of mitochondrial dynamics can help in developing new therapies for the treatment of these conditions. In this review, we summarize the recent knowledge on the processes of mitochondrial turnover and the proteins and genes involved in it. We provide a list of known mutations that affect mitochondrial function, and discuss the emerging therapeutic approaches.

Indexed as

atherosclerosisinflammationmitochondrial dynamicsmitochondrionmtDNA mutationoxidative stress

Identifiers

PMID33672784
PMCPMC7924632
OpenAlexW3130092766

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.