ArticleThe American journal of pathology1998
ACE inhibitor quinapril reduces the arterial expression of NF-kappaB-dependent proinflammatory factors but not of collagen I in a rabbit model of atherosclerosis.
Article in The American journal of pathology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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.
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.
Who cites it
21 citing papers in PubMed, 122 citations in OpenAlex.
- A Five-Year Prospective, Randomized, Open-Label Study of Standard-Dose Versus Low-Dose Prolonged-Release Tacrolimus With or Without Angiotensin-Converting Enzyme Inhibitor or Angiotensin II Receptor Blocker Post Kidney Transplantation.Clinical transplantation · 2025Trial
- Impact of angiotensin converting enzyme inhibition on post-coronary artery bypass interleukin 6 release.Heart (British Cardiac Society) · 2002Trial
- Exploring Negative Feedback Mechanisms in the PTEN-ACE Axis: Application of Electrosorb Hydrogel-Based Gene Delivery for Intervertebral Disc Regeneration.International journal of biological sciences · 2025Article
- NF-kB affects migration of vascular smooth muscle cells after treatment with heparin and ibrutinib.Biochemistry and biophysics reports · 2024Article
- Blocking TNF signaling may save lives in COVID-19 infection.Molecular biology reports · 2022Review
- COVID-19: the role of excessive cytokine release and potential ACE2 down-regulation in promoting hypercoagulable state associated with severe illness.Journal of thrombosis and thrombolysis · 2021Review
- Suppression of Remodeling Behaviors with Arachidonic Acid Modification for Enhanced in vivo Antiatherogenic Efficacies of Lovastatin-loaded Discoidal Recombinant High Density Lipoprotein.Pharmaceutical research · 2015Article
- Enalapril stimulates collagen biosynthesis through prolidase-dependent mechanism in cultured fibroblasts.Naunyn-Schmiedeberg's archives of pharmacology · 2015Article
- ACE inhibitors potently reduce vascular inflammation, results of an open proof-of-concept study in the abdominal aortic aneurysm.PloS one · 2014Article
- Angiotensin II is a new component involved in splenic T lymphocyte responses during Plasmodium berghei ANKA infection.PloS one · 2013Article
- Clarifying off-target effects for torcetrapib using network pharmacology and reverse docking approach.BMC systems biology · 2012Article
- The effect of azithromycin on the maturation and function of murine bone marrow-derived dendritic cells.Clinical and experimental immunology · 2011Article
- Captopril reduces cardiac inflammatory markers in spontaneously hypertensive rats by inactivation of NF-kB.Journal of inflammation (London, England) · 2010Article
- Common pathways of hypercholesterolemia and hypertension leading to atherothrombosis: the need for a global approach in the management of cardiovascular risk factors.Vascular health and risk management · 2007Review
- C reactive protein concentration and recurrence of atrial fibrillation after electrical cardioversion.Heart (British Cardiac Society) · 2005Article
- Inflammation and atherosclerosis.Current atherosclerosis reports · 2004Review
- Reduction of bleomycin induced lung fibrosis by candesartan cilexetil, an angiotensin II type 1 receptor antagonist.Thorax · 2004Article
- Angiotensin II induced inflammation in the kidney and in the heart of double transgenic rats.BMC cardiovascular disorders · 2002Article
- Angiotensin, inflammation, hypertension, and cardiovascular disease.Current hypertension reports · 2001Review
- Regulation of matrix proteins and impact on vascular structure.Current hypertension reports · 2000Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Increasing evidence supports an association between inflammation and plaque rupture. Macrophages and vascular smooth muscle cells are a source of cytokines and growth factors, which contribute to ongoing inflammation during atherogenesis. In a rabbit model of atherosclerosis, we evaluated the effect of the ACE inhibitor quinapril on different parameters implicated in the pathogenesis of the plaque, such as the presence of chemokines (interleukin-8, monocyte chemoattractant protein-1), collagen I, and vascular smooth muscle cell proliferation (PDGF-B). Since nuclear factor kappaB (NF-kappaB) has been implicated in the control of chemokine transcription and cell proliferation, we also investigated its activation and localization in the lesion. Quinapril administration for 28 days caused a down-regulation in arterial expression of interleukin-8 and monocyte chemoattractant protein-1 (mRNA and protein). However, collagen I expression (mRNA and protein) was not modified. PDGF-B expression was reduced in both the intima and the media. Active NF-kappaB, found in both macrophages and vascular smooth muscle cells, was also reduced by quinapril. Nevertheless, no significant changes were noted in the mild neointima formation, although a certain trend toward normalization was found in the quinapril-treated group. In conclusion, our results show that quinapril treatment attenuates several parameters associated with inflammation within the atherosclerotic lesions that are controlled by NF-kappaB, although it has no effect on collagen I expression. Both effects could contribute to the stabilization of the atherosclerotic plaque.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.