Evidence map›Paper›PMID 25741283›Full record

ReviewFrontiers in physiology2015

Nitric oxide and mitochondria in metabolic syndrome.

Larisa Litvinova, Dmitriy N Atochin, Nikolai Fattakhov, Mariia Vasilenko, Pavel Zatolokin, Elena Kirienkova

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
6.8field-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

63 citing papers in PubMed, 125 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Trial
  4. Article
  5. Nanomedicines Against Mitochondrial Dysfunction-Induced Metabolic Diseases.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. Targeting L-arginine/NO/cGMP/KFrontiers in pharmacology · 2025
    Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Review
  19. Why Are Perivascular Spaces Important?Medicina (Kaunas, Lithuania) · 2023
    Review
  20. Review

3 more citing papers are in PubMed but not listed here.

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 3 institutions in 2 countries.

Larisa LitvinovaLaboratory of Immunology and Cellular Biotechnologies, Innovation Park of the Immanuel Kant Baltic Federal University Kaliningrad, Russia.
Dmitriy N AtochinCardiology Division, Department of Medicine, Cardiovascular Research Center, Harvard Medical School, Massachusetts General Hospital Boston, MA, USA.
Nikolai FattakhovLaboratory of Immunology and Cellular Biotechnologies, Innovation Park of the Immanuel Kant Baltic Federal University Kaliningrad, Russia.
Mariia VasilenkoLaboratory of Immunology and Cellular Biotechnologies, Innovation Park of the Immanuel Kant Baltic Federal University Kaliningrad, Russia.
Pavel ZatolokinDepartment of Reconstructive and Endoscopic Surgery, Kaliningrad Regional Hospital Kaliningrad, Russia.
Elena KirienkovaLaboratory of Immunology and Cellular Biotechnologies, Innovation Park of the Immanuel Kant Baltic Federal University Kaliningrad, Russia.
Immanuel Kant Baltic Federal University · RUKaliningrad State Technical University · RUMassachusetts General Hospital · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metabolic syndrome (MS) is a cluster of metabolic disorders that collectively increase the risk of cardiovascular disease. Nitric oxide (NO) plays a crucial role in the pathogeneses of MS components and is involved in different mitochondrial signaling pathways that control respiration and apoptosis. The present review summarizes the recent information regarding the interrelations of mitochondria and NO in MS. Changes in the activities of different NO synthase isoforms lead to the formation of metabolic disorders and therefore are highlighted here. Reduced endothelial NOS activity and NO bioavailability, as the main factors underlying the endothelial dysfunction that occurs in MS, are discussed in this review in relation to mitochondrial dysfunction. We also focus on potential therapeutic strategies involving NO signaling pathways that can be used to treat patients with metabolic disorders associated with mitochondrial dysfunction. The article may help researchers develop new approaches for the diagnosis, prevention and treatment of MS.

Indexed as

metabolic syndromemitochondrial dysfunctionmitochondrial nitric oxide synthasenitric oxidenitric oxide synthasenitric oxide synthase type Initric oxide synthase type IIoxide synthase type III

Identifiers

PMID25741283
PMCPMC4330700
OpenAlexW2045176648

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.