Evidence map›Paper›PMID 26225968›Full record

ReviewInternational journal of molecular sciences2015

Advances in the Study of the Antiatherogenic Function and Novel Therapies for HDL.

Peiqiu Cao, Haitao Pan, Tiancun Xiao, Ting Zhou, Jiao Guo, Zhengquan Su

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.9field-weighted citation impact, top 24% 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

4 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
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

6 authors at 3 institutions in 2 countries.

Peiqiu CaoKey Research Center of Liver Regulation for Hyperlipemia SATCM/Class III, Laboratory of Metabolism SATCM, Guangdong TCM Key Laboratory for Metabolic Diseases, Guangdong Pharmaceutical University, Guangzhou 510006, China. cpq_520@126.com.
Haitao PanKey Research Center of Liver Regulation for Hyperlipemia SATCM/Class III, Laboratory of Metabolism SATCM, Guangdong TCM Key Laboratory for Metabolic Diseases, Guangdong Pharmaceutical University, Guangzhou 510006, China. pangel7835001@163.com.
Tiancun XiaoInorganic Chemistry Laboratory, University of Oxford, South Parks Road, Oxford OX1 3QR, UK. ting4677@126.com.
Ting ZhouGuangzhou Boxabio Ltd., D-106 Guangzhou International Business Incubator, Guangzhou 510530, China. ting4677@126.com.
Jiao GuoKey Research Center of Liver Regulation for Hyperlipemia SATCM/Class III, Laboratory of Metabolism SATCM, Guangdong TCM Key Laboratory for Metabolic Diseases, Guangdong Pharmaceutical University, Guangzhou 510006, China. wshxalb@163.com.
Zhengquan SuKey Research Center of Liver Regulation for Hyperlipemia SATCM/Class III, Laboratory of Metabolism SATCM, Guangdong TCM Key Laboratory for Metabolic Diseases, Guangdong Pharmaceutical University, Guangzhou 510006, China. suzhq@scnu.edu.cn.
Guangdong Pharmaceutical University · CNState Administration of Traditional Chinese Medicine of the People's Republic of China · CNUniversity of Oxford · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The hypothesis that raising high-density lipoprotein cholesterol (HDL-C) levels could improve the risk for cardiovascular disease (CVD) is facing challenges. There is multitudinous clear clinical evidence that the latest failures of HDL-C-raising drugs show no clear association with risks for CVD. At the genetic level, recent research indicates that steady-state HDL-C concentrations may provide limited information regarding the potential antiatherogenic functions of HDL. It is evident that the newer strategies may replace therapeutic approaches to simply raise plasma HDL-C levels. There is an urgent need to identify an efficient biomarker that accurately predicts the increased risk of atherosclerosis (AS) in patients and that may be used for exploring newer therapeutic targets. Studies from recent decades show that the composition, structure and function of circulating HDL are closely associated with high cardiovascular risk. A vast amount of data demonstrates that the most important mechanism through which HDL antagonizes AS involves the reverse cholesterol transport (RCT) process. Clinical trials of drugs that specifically target HDL have so far proven disappointing, so it is necessary to carry out review on the HDL therapeutics.

Indexed as

AnimalsAnticholesteremic AgentsAtherosclerosisBiomarkersCholesterol, HDLHumansHypercholesterolemiaAnticholesteremic AgentsBiomarkersCholesterol, HDLbiomarkerHDLHDL functionHDL therapiesreverse cholesterol transport

Identifiers

PMID26225968
PMCPMC4581191
OpenAlexW2142168749

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.