ReviewCurrent cardiology reports2011
Apo a-I modulating therapies.
Review in Current cardiology reports, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed.
- Trial
- High residual cardiovascular risk after lipid-lowering: prime time for Predictive, Preventive, Personalized, Participatory, and Psycho-cognitive medicine.Frontiers in cardiovascular medicine · 2023Review
- Short term resistance training enhanced plasma apoA-I and FABP4 levels in Streptozotocin-induced diabetic rats.Journal of diabetes and metabolic disorders · 2014Article
- Genome-wide screen for modulation of hepatic apolipoprotein A-I (ApoA-I) secretion.The Journal of biological chemistry · 2013Article
- Xanthohumol prevents atherosclerosis by reducing arterial cholesterol content via CETP and apolipoprotein E in CETP-transgenic mice.PloS one · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The substantial residual risk of cardiovascular events despite the implementation of effective lowering of low-density lipoprotein cholesterol highlights the need to develop additional cardioprotective therapies. Evidence from population and animal studies suggests that high-density lipoproteins (HDLs), the protective lipid particles, may represent a target for therapeutic modification. As a result intensive efforts are in progress to develop new agents that promote HDL activity. Among these different approaches, a range of strategies that target apolipoprotein A-I, the major protein carried on HDL, are being evaluated.
Indexed as
Identifiers
21947768What 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.