Evidence map›Paper›PMID 32570831›Full record

ReviewBiomedicines2020

Mitochondrial Dysfunction and DNA Damage in the Context of Pathogenesis of Atherosclerosis.

Taisiia Shemiakova, Ekaterina Ivanova, Andrey V Grechko, Elena V Gerasimova, Igor A Sobenin, Alexander N Orekhov

Open access · goldAbstract readReview
In one paragraph

Review in Biomedicines, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

44 citing papers in PubMed, 85 citations in OpenAlex.

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  17. Neutrophil extracellular traps: a catalyst for atherosclerosis.Molecular and cellular biochemistry · 2024
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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

6 authors at 6 institutions in 1 country.

Taisiia ShemiakovaInstitute of Translational Biomedicine, St. Petersburg State University, 199034 St. Petersburg, Russia.ORCID 0000-0001-8618-7942
Ekaterina IvanovaDepartment of Basic Research, Institute for Atherosclerosis Research, 121609 Moscow, Russia.ORCID 0000-0003-3159-2881
Andrey V GrechkoFederal Scientific Clinical Center for Resuscitation and Rehabilitation, 109240 Moscow, Russia.
Elena V GerasimovaLaboratory of Systemic Rheumatic Disorders, V.A. Nasonova Institute of Rheumatology, 115522 Moscow, Russia.ORCID 0000-0001-5815-561X
Igor A SobeninLaboratory of Medical Genetics, Institute of Experimental Cardiology, National Medical Research Center of Cardiology, 121552 Moscow, Russia.ORCID 0000-0003-0978-6444
Alexander N OrekhovLaboratory of Angiopathology, Institute of General Pathology and Pathophysiology, 125315 Moscow, Russia.ORCID 0000-0002-3318-4681
Association of Rheumatologists of Russia · RUInstitute for Atherosclerosis Research · RUInstitute of Experimental Cardiology · RUResearch Institute of General Pathology and Pathophysiology, the Russian Academy of Medical Sciences · RUSt Petersburg University · RUV.A. Negovsky Scientific Research Institute of General Reanimatology · RU

Funding

Russian Science Foundation 19-15-00297
6 · The paper itself

Abstract

Atherosclerosis is a multifactorial disease of the cardiovascular system associated with aging, inflammation, and oxidative stress. An important role in the development of atherosclerosis play elevated plasma lipoproteins. A number of external factors (smoking, diabetes, infections) can also contribute to the development of the disease. For a long time, atherosclerosis remains asymptomatic, therefore, the search for early markers of the disease is critical for the timely management and better outcomes for patients. Mitochondrial dysfunction and mitochondrial DNA (mtDNA) damage appear to connect different aspects of atherosclerosis pathogenesis. To date, multiple lines of research have demonstrated the strong association of mitochondrial dysfunction with the development of various human diseases. Therapies aimed at restoring the mitochondrial function are being actively developed, and are expected to broaden the therapeutic possibilities for several chronic human diseases. The development of such therapies depends on our understanding of the functional roles of different mtDNA variants associated with one or another disorder, and the molecular mechanisms linking mitochondrial dysfunction with a given pathological feature. These questions are, however, challenging and require future intensive research. This review summarizes the recent studies and describes the central processes of the development of atherosclerosis, and shows their relationship with mitochondrial dysfunction. One of the promising therapeutic approaches for future atherosclerosis treatments is the use of mitochondria-targeted antioxidants. Future studies should focus on characterizing the mechanisms of mitochondrial involvement in cardiovascular pathologies to better direct the search for novel therapies.

Indexed as

antioxidantsatherosclerosisendothelial cellsinflammationmitochondrial dysfunctionmtDNA damageoxidative stress

Identifiers

PMID32570831
PMCPMC7344998
OpenAlexW3036253915

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.