Evidence map›Paper›PMID 38216994›Full record

ArticleLipids in health and disease2024

Unlocking the mysteries of VLDL: exploring its production, intracellular trafficking, and metabolism as therapeutic targets.

Jingfei Chen, Zhenfei Fang, Qin Luo, Xiao Wang, Mohamad Warda, Avash Das, Federico Oldoni, Fei Luo

Abstract read
In one paragraph

Article in Lipids in health and disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

25 citing papers in PubMed, 2 syntheses or guidelines pooled it.

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  10. NSAIDs beyond COX:ACS omega · 2025
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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

8 authors.

Jingfei ChenReproductive Medicine Center, Department of Obstetrics and Gynecology, Research Institute of Blood Lipid and Atherosclerosis, The Second Xiangya Hospital, Central South University, Changsha, Hunan, 410011, China.
Zhenfei FangResearch Institute of Blood Lipid and Atherosclerosis, the Second Xiangya Hospital, Central South University, Changsha, Hunan, 410011, China.
Qin LuoResearch Institute of Blood Lipid and Atherosclerosis, the Second Xiangya Hospital, Central South University, Changsha, Hunan, 410011, China.
Xiao WangState Key Laboratory of Membrane Biology, Peking University, Beijing, 100871, China.
Mohamad WardaDepartment of Biochemistry and Molecular Biology, Faculty of Veterinary Medicine, Cairo University, Giza, 12211, Egypt.
Avash DasDepartment of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, 02215-5400, USA.
Federico OldoniDepartment of Molecular Genetics, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Fei LuoResearch Institute of Blood Lipid and Atherosclerosis, the Second Xiangya Hospital, Central South University, Changsha, Hunan, 410011, China. luofei0058@csu.edu.cn.

Funding

Hunan Provincial Natural Science Foundation of China 2021JJ40852Hunan Provincial Natural Science Foundation of China 2022JJ40675Key Research and Development Program of Hunan Province of China 2021SK2004National Natural Science Foundation of China 82100495National Natural Science Foundation of China 82201879Scientific Research Project of Hunan Provincial Health Commission 202203014009Scientific Research Project of Hunan Provincial Health Commission 202305037231
6 · The paper itself

Abstract

Reducing circulating lipid levels is the centerpiece of strategies for preventing and treating atherosclerotic cardiovascular disease (ASCVD). Despite many available lipid-lowering medications, a substantial residual cardiovascular risk remains. Current clinical guidelines focus on plasma levels of low-density lipoprotein (LDL). Recent attention has been given to very low-density lipoprotein (VLDL), the precursor to LDL, and its role in the development of coronary atherosclerosis. Preclinical investigations have revealed that interventions targeting VLDL production or promoting VLDL metabolism, independent of the LDL receptor, can potentially decrease cholesterol levels and provide therapeutic benefits. Currently, methods, such as mipomersen, lomitapide, and ANGPTL3 inhibitors, are used to reduce plasma cholesterol and triglyceride levels by regulating the lipidation, secretion, and metabolism of VLDL. Targeting VLDL represents an avenue for new lipid-lowering strategies. Interventions aimed at reducing VLDL production or enhancing VLDL metabolism, independent of the LDL receptor, hold promise for lowering cholesterol levels and providing therapeutic benefits beyond LDL in the management of ASCVD.

Indexed as

AtherosclerosisLipoproteins, VLDLAngiopoietin-Like Protein 3CholesterolHumansLipoproteins, LDLReceptors, LDLAngiopoietin-Like Protein 3ANGPTL3 protein, humanCholesterolLipoproteins, LDLLipoproteins, VLDLReceptors, LDLAtherosclerotic cardiovascular diseaseLDL receptor-independent pathwayLow-density lipoproteinVery low-density lipoprotein

Identifiers

PMID38216994
PMCPMC10785355

What Socratic 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 Socratic graph.