ArticleMolecular medicine reports2016
Atorvastatin attenuates p‑cresyl sulfate‑induced atherogenesis and plaque instability in ApoE knockout mice.
Article in Molecular medicine reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 11 citations in OpenAlex.
- Targeting Uremic Toxins in Chronic Kidney Disease: Current Challenges and Emerging Therapeutic Strategies.Toxins · 2026Review
- The AKI-to-CKD Transition: The Role of Uremic Toxins.International journal of molecular sciences · 2023Review
- Tongxinluo enhances the effect of atorvastatin on the treatment of atherosclerosis with chronic obstructive pulmonary disease by maintaining the pulmonary microvascular barrier.Food science & nutrition · 2023Article
- Uremic Toxins: An Alarming Danger Concerning the Cardiovascular System.Frontiers in physiology · 2021Review
- Uremic Toxins and Vascular Dysfunction.Toxins · 2020Review
- Gut-Derived Metabolites and Their Role in Immune Dysfunction in Chronic Kidney Disease.Toxins · 2020Review
- Short‑term use of atorvastatin affects glucose homeostasis and suppresses the expression of LDL receptors in the pancreas of mice.Molecular medicine reports · 2018Article
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
p-cresyl sulfate (PCS) is a protein-bound uremic toxin retained in the blood of patients with chronic kidney disease (CKD) As atherosclerosis is a primary cardiovascular complication for patients with CKD, the aim of the present study was to investigate the mechanisms underlying the aggravation of atherosclerosis by PCS. In addition, the effect of atorvastatin was assessed in reversing the effects of PCS. PCS was revealed to promote the initiation and progression of atherosclerosis. Following treatment with atorvastatin, apolipoprotein E knockout mice demonstrated a reduction in PCS‑induced atherogenesis and plaque vulnerability. In addition, atorvastatin decreased the protein expression levels of vascular cell adhesion molecule‑1 and intercellular cell adhesion molecule‑1, and the interaction between leukocytes and endothelia. The plasma lipid profiles of mice were not significantly affected by gavage of low‑dose atorvastatin. The results of the present study indicate that PCS promotes plaque growth and instability by enhancing leukocyte‑endothelium interaction, and that these effects may be attenuated by atorvastatin treatment.
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.