Evidence map›Paper›PMID 36232471›Full record

ReviewInternational journal of molecular sciences2022

Lipopolysaccharides and Cellular Senescence: Involvement in Atherosclerosis.

Kaori Suzuki, Etsuo A Susaki, Isao Nagaoka

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.5field-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

34 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Correlation Between Dysbiosis and Atrial Fibrillation: What's New?International journal of molecular sciences · 2025
    Review
  12. The Emerging Role of Senolysis in Atherosclerosis.Medicina (Kaunas, Lithuania) · 2025
    Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review
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

3 authors at 1 institution in 1 country.

Kaori SuzukiDepartment of Host Defense and Biochemical Research, Juntendo University Graduate School of Medicine, Bunkyo-ku 113-8421, Tokyo, Japan.ORCID 0000-0002-2048-866X
Etsuo A SusakiDepartment of Biochemistry and Systems Biomedicine, Juntendo University Graduate School of Medicine, Bunkyo-ku 113-8421, Tokyo, Japan.ORCID 0000-0001-5621-7311
Isao NagaokaDepartment of Host Defense and Biochemical Research, Juntendo University Graduate School of Medicine, Bunkyo-ku 113-8421, Tokyo, Japan.ORCID 0000-0003-0824-7406
Juntendo University · JP

Funding

Japan Agency for Medical Research and Development JP22gm6210027Japan Society for the Promotion of Science 22H02824Strategic Research Foundation Grant-aided Project for Private Universities Grant Number: S1411007
6 · The paper itself

Abstract

Atherosclerosis is a chronic inflammatory disease of the vascular walls related to aging. Thus far, the roles of cellular senescence and bacterial infection in the pathogenesis of atherosclerosis have been speculated to be independent of each other. Some types of macrophages, vascular endothelial cells, and vascular smooth muscle cells are in a senescent state at the sites of atherosclerotic lesions. Likewise, bacterial infections and accumulations of lipopolysaccharide (LPS), an outer-membrane component of Gram-negative bacteria, have also been observed in the atherosclerotic lesions of patients. This review introduces the integration of these two potential pathways in atherosclerosis. Previous studies have suggested that LPS directly induces cellular senescence in cultured monocytes/macrophages and vascular cells. In addition, LPS enhances the inflammatory properties (senescence-associated secretory phenotype [SASP]) of senescent endothelial cells. Thus, LPS derived from Gram-negative bacteria could exaggerate the pathogenesis of atherosclerosis by inducing and enhancing cellular senescence and the SASP-associated inflammatory properties of specific vascular cells in atherosclerotic lesions. This proposed mechanism can provide novel approaches to preventing and treating this common age-related disease.

Indexed as

AtherosclerosisLipopolysaccharidesCellular SenescenceEndothelial CellsHumansLipopolysaccharidesatherosclerosiscellular senescenceendothelial cellslipopolysaccharide (LPS)senescence-associated secretory phenotype (SASP)

Identifiers

PMID36232471
PMCPMC9569556
OpenAlexW4296993555

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.