Evidence map›Paper›PMID 18274671›Full record

ArticleThe Journal of clinical investigation2008

Renin inhibition reduces hypercholesterolemia-induced atherosclerosis in mice.

Hong Lu, Debra L Rateri, David L Feldman, Richard J Charnigo, Akiyoshi Fukamizu, Junji Ishida, Elizabeth G Oesterling, Lisa A Cassis, Alan Daugherty

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed, 1 pooled it
16.2field-weighted citation impact, top 1% 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

83 citing papers in PubMed, 1 synthesis or guideline pooled it, 208 citations in OpenAlex.

  1. Direct Vascular Effects of Angiotensin II (A Systematic Short Review).International journal of molecular sciences · 2024
    Pooled it
  2. Trial
  3. Trial
  4. Trial
  5. Trial
  6. Observational
  7. Article
  8. Observational
  9. Angiotensinogen as a Therapeutic Target for Cardiovascular and Metabolic Diseases.Arteriosclerosis, thrombosis, and vascular biology · 2024
    Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Endocytic Adaptors in Cardiovascular Disease.Frontiers in cell and developmental biology · 2020
    Review
  17. Article
  18. Updates on Approaches for Studying Atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2019
    Article
  19. Angiotensinogen and Megalin Interactions Contribute to Atherosclerosis-Brief Report.Arteriosclerosis, thrombosis, and vascular biology · 2019
    Article
  20. Review

23 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

9 authors at 3 institutions in 1 country.

Hong LuCardiovascular Research Center, University of Kentucky, Lexington, Kentucky, USA.
Debra L Rateri
David L Feldman
Richard J Charnigo
Akiyoshi Fukamizu
Junji Ishida
Elizabeth G Oesterling
Lisa A Cassis
Alan Daugherty
University of Kentucky · USThe Graduate Center, CUNY · USNovartis (United States) · US

Funding

Sources and effects of angiotensin peptides in atherosclerosisR01HL062846 · NHLBI · UNIVERSITY OF KENTUCKY · PI DAUGHERTY, ALAN · 2000 to 2012
$2.8M
NHLBI NIH HHS HL62846NHLBI NIH HHS R01 HL062846
6 · The paper itself

Abstract

The role of the renin angiotensin system (RAS) in atherosclerosis is complex because of the involvement of multiple peptides and receptors. Renin is the rate-limiting enzyme in the production of all angiotensin peptides. To determine the effects of renin inhibition on atherosclerosis, we administered the novel renin inhibitor aliskiren over a broad dose range to fat-fed LDL receptor-deficient (Ldlr(-/-)) mice. Renin inhibition resulted in striking reductions of atherosclerotic lesion size in both the aortic arch and the root. Subsequent studies demonstrated that cultured macrophages expressed all components of the RAS. To determine the role of macrophage-derived angiotensin in the development of atherosclerosis, we transplanted renin-deficient bone marrow to irradiated Ldlr(-/-) mice and observed a profound decrease in the size of atherosclerotic lesions. In similar experiments, transplantation of bone marrow deficient for angiotensin II type 1a receptors failed to influence lesion development. We conclude that renin-dependent angiotensin production in macrophages does not act in an autocrine/paracrine manner. Furthermore, in vitro studies demonstrated that coculture with renin-expressing macrophages augmented monocyte adhesion to endothelial cells. Therefore, although previous work suggests that angiotensin peptides have conflicting effects on atherogenesis, we found that renin inhibition profoundly decreased lesion development in mice.

Indexed as

Renin InhibitorsAmidesAnimalsAtherosclerosisBone Marrow TransplantationCell AdhesionCells, CulturedFumaratesHypercholesterolemiaMacrophagesMiceMice, Inbred C57BLMonocytesReceptor, Angiotensin, Type 1Receptors, LDLSystolealiskirenAmidesFumaratesReceptor, Angiotensin, Type 1Receptors, LDLRenin Inhibitors

Identifiers

PMID18274671
PMCPMC2242618
OpenAlexW2075120792

What OpenQuestion holds

Textmetadata
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.