Evidence map›Paper›PMID 35064467›Full record

ReviewJournal of physiology and biochemistry2022

A novel therapeutic strategy for atherosclerosis: autophagy-dependent cholesterol efflux.

Haipeng Guo, Dongmei Wei, Rui Liu, Chao Zhang, Song Jiang, Weijia Wang, Hongzhe Hu, Lijuan Shen, Xiaofei Liang

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of physiology and biochemistry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

8 citing papers in PubMed, 14 citations in OpenAlex.

  1. mFrontiers in immunology · 2026
    Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Blocking HJournal of molecular medicine (Berlin, Germany) · 2024
    Article
  8. Review
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

9 authors at 3 institutions in 1 country.

Haipeng GuoDepartment of Laboratory Medicine, The First Hospital of Qiqihar, Qiqihar, 161005, China.
Dongmei WeiDepartment of Traditional Chinese Geriatric Medicine, The First Hospital of Qiqihar, Qiqihar, 161005, China.
Rui LiuMinistry of Science and Education, The First Hospital of Qiqihar, Qiqihar, 161005, China.
Chao ZhangDepartment of Laboratory Medicine, The First Hospital of Qiqihar, Qiqihar, 161005, China.
Song JiangDepartment of Laboratory Medicine, The First Hospital of Qiqihar, Qiqihar, 161005, China.
Weijia WangDepartment of Laboratory Medicine, The First Hospital of Qiqihar, Qiqihar, 161005, China.
Hongzhe HuDepartment of Laboratory Medicine, The First Hospital of Qiqihar, Qiqihar, 161005, China.
Lijuan ShenQiqihar MingZhu Hospital, Qiqihar, 161000, China.
Xiaofei LiangDepartment of Laboratory Medicine, The First Hospital of Qiqihar, Qiqihar, 161005, China. liangxiaofeidoctor@163.com.ORCID http://orcid.org/0000-0001-7696-6571
Southern Medical University · CNQiqihar Medical University · CNQiqihar University · CN

Funding

the nature science foundation of heilongjiang province No. LH2020H137
6 · The paper itself

Abstract

Atherosclerosis (AS) is a chronic inflammatory disease characterized by abnormal lipid metabolism. Foam cell formation is also known as an early event of AS. Cholesterol efflux is a process whereby cholesterol is excreted from foam cells through transporters, which serves as one of the effective regulatory mechanisms to prevent AS. Autophagy is a biodegradable mechanism, and lipophagy is a special form of autophagy that selectively degrades lipids. Cholesterol efflux is regulated by several mechanisms. Moreover, numerous studies have shown that autophagy is also process whereby cholesterol efflux is regulated. In early studies, scholars found that cholesterol efflux is related to autophagy. Subsequent studies have shown that various targeted molecules can induce autophagy and promote the expression of cholesterol transporters (such as LXRα, ABCA1, and ABCG1) through specific signaling pathways. Several novel treatments for AS use these small molecules as entry points for research and development based on autophagy. However, this autophagy-dependent cholesterol efflux involves many different molecular mechanisms. This not only indicates that cholesterol efflux is the result of multiple factors, but also that autophagy, which mediates cholesterol efflux, is a complex physiological mechanism. Through a literature review, we found that the role of autophagy in cholesterol efflux is related to cell type and is regulated by both the level of autophagy and the mechanism that triggers autophagy. In this review, we aim to discuss the role of autophagy in cholesterol efflux from many aspects based on recent relevant studies to aid in the treatment of AS.

Indexed as

AtherosclerosisFoam CellsATP Binding Cassette Transporter 1AutophagyCholesterolHumansLiver X ReceptorsATP Binding Cassette Transporter 1CholesterolLiver X ReceptorsABCA1ABCG1AtherosclerosisAutophagyCholesterol effluxFoam cell

Identifiers

PMID35064467
OpenAlexW4206970938

What OpenQuestion holds

Textmetadata
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.