Evidence map›Paper›PMID 26712802›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2015

Niacin Suppresses Progression of Atherosclerosis by Inhibiting Vascular Inflammation and Apoptosis of Vascular Smooth Muscle Cells.

Gang Su, Guangli Sun, Hai Liu, Liliang Shu, Jingchao Zhang, Longhui Guo, Chen Huang, Jing Xu

Open access · hybridAbstract read
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.1field-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

25 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. NADSub-cellular biochemistry · 2024
    Review
  6. Article
  7. Article
  8. Tackling Atherosclerosis via Selected Nutrition.International journal of molecular sciences · 2022
    Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Molecular mechanisms and genetic regulation in atherosclerosis.International journal of cardiology. Heart & vasculature · 2018
    Review
  18. Article
  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

8 authors at 1 institution in 1 country.

Gang SuDepartment of Cardiovascular Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China (mainland).
Guangli SunDepartment of Ophthalmology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China (mainland).
Hai LiuDepartment of Cardiovascular Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China (mainland).
Liliang ShuDepartment of Cardiovascular Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China (mainland).
Jingchao ZhangDepartment of Cardiovascular Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China (mainland).
Longhui GuoDepartment of Cardiovascular Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China (mainland).
Chen HuangDepartment of Cardiovascular Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China (mainland).
Jing XuDepartment of Cardiovascular Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China (mainland).
First Affiliated Hospital of Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND Niacin is a broad-spectrum lipid-regulating drug used for the clinical therapy of atherosclerosis; however, the mechanisms by which niacin ameliorates atherosclerosis are not clear. MATERIAL AND METHODS The effect of niacin on atherosclerosis was assessed by detection of atherosclerotic lesion area. Adhesion molecules in arterial endothelial cells were determined by using qRT-PCR and Western blot analysis. The levels of serum inflammatory cytokines in ApoE-/- mice were detected by using ELISA. We detected the expression levels of phosphorylated nuclear factors-kB (NF-κB) p65 in aortic endothelial cells of mice using Western blot analysis. Furthermore, we investigated the anti-inflammation effect and endothelium-protecting function of niacin and their regulatory mechanisms in vitro. RESULTS Niacin inhibited the progress of atherosclerosis and decreased the levels of serum inflammatory cytokines and adhesion molecules in ApoE-/- mice. Niacin suppressed the activity of NF-κB and apoptosis of vascular smooth muscle cells (VSMCs). Furthermore, niacin induced phosphorylated focal adhesion kinase (FAK) and FAK inhibitor PF-573228 reduced the level of Bcl-2 and elevated the level of cleaved caspase-3 in VSMCs. CONCLUSIONS Niacin inhibits vascular inflammation and apoptosis of VSMCs via inhibiting the NF-κB signaling and the FAK signaling pathway, respectively, thus protecting ApoE-/- mice against atherosclerosis.

Indexed as

AnimalsApolipoproteins EApoptosisAtherosclerosisCell Adhesion MoleculesCells, CulturedCytokinesInflammationMaleMiceMice, Inbred C57BLMice, TransgenicMuscle, Smooth, VascularNF-kappa BNiacinSignal TransductionApolipoproteins ECell Adhesion MoleculesCytokinesNF-kappa BNiacinTumor Necrosis Factor-alpha

Identifiers

PMID26712802
PMCPMC4699630
OpenAlexW2213695532

What OpenQuestion holds

Texttitle and abstract
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.