Cited by 54Apelin-related biomedical researchCholesterol and Lipid MetabolismAtherosclerosis and Cardiovascular Diseases

RETRACTED: Apelin-13 impedes foam cell formation by activating Class III PI3K/Beclin-1-mediated autophagic pathway

Yao, Feng, Lv, Yun-Cheng, Zhang, Min, Xie, Wei, Tan, Yu-Lin, Gong, Duo, Cheng, Hai-Peng, Liu, Dan +4 more·2015·Biochemical and Biophysical Research Communications

Abstract

Apelin-13, an adipokine, promotes cholesterol efflux in macrophages with antiatherosclerotic effect. Autophagy, an evolutionarily ancient response to cellular stress, has been involved in atherosclerosis. Therefore, the purpose of this study was to investigate whether apelin-13 regulates macrophage foam cell cholesterol metabolism through autophagy, and also explore the underlying mechanisms. Here, we revealed that apelin-13 decreased lipid accumulation in THP-1 derived macrophages through markedly enhancing cholesterol efflux. Our study further demonstrated that apelin-13 induced autophagy via activation of Class III phosphoinositide 3-kinase (PI3K) and Beclin-1. Inhibition of Class III PI3K and Beclin-1 suppressed the stimulatory effects of apelin-13 on autophagy activity. The present study concluded that apelin-13 reduces lipid accumulation of foam cells by activating autophagy via Class III PI3K/Beclin-1 pathway. Therefore, our results provide brand new insight about apelin-13 inhibiting foam cell formation and highlight autophagy as a promising therapeutic target in atherosclerosis.

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Crossref · 10.1016/j.bbrc.2015.09.045This paper is marked retracted.

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  • In vitro studies using human cells and tissues indicate that apelin-13 improves lipid metabolism, exerts anti-inflammatory effects by inhibiting IL-6, IL-1β, and TNF-α, and may help stabilize atherosclerotic plaques.

    “In vitro studies using human cells and tissues indicate that apelin-13 improves lipid metabolism [62], exerts anti-inflammatory effects by inhibiting IL-6, IL-1β, and TNF-α, and may help stabilize atherosclerotic plaques [62,63].”
  • Apelin-13 and its analogs are being explored for cardiovascular protection, given their ability to improve lipid metabolism, exert anti-inflammatory effects, and stabilize atherosclerotic plaques.

    “Similarly, apelin-13 and its analogs are being explored for cardiovascular protection, given their ability to improve lipid metabolism, exert anti-inflammatory effects, and stabilize atherosclerotic plaques [62,63].”

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Authors
Yao, F., Lv, Y.-C., Zhang, M., Xie, W., Tan, Y.-L., Gong, D., Cheng, H.-P., Liu, D., Li, L., Liu, X.-Y., Zheng, X.-L., & Tang, C.-K.
Affiliations
  • University of South China (CN)
  • University of Calgary (CA)
Corresponding author
Tang, Chao-Ke
Venue
Biochemical and Biophysical Research Communications
Publisher
Elsevier BV
Published
2015-10
Volume
466
Issue
4
Pages
637-643
ISSN
0006-291X (ISSN-L)
OpenAlex
W1665898857
Cited by
54
References
38
Citations by year
2026: 3 · 2025: 6 · 2024: 2 · 2023: 3 · 2022: 4 · 2021: 4 · 2020: 6 · 2019: 5 · 2018: 10 · 2017: 8 · 2016: 3
FWCI
5.03
Type
journal article
Language
en
Status
Retracted
Open access
closed
Locations
  • Biochemical and Biophysical Research Communications (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Natural Science Foundation of China (81170278, 81300224, 81370377)
  • University of South China (2014-004)
  • Science and Technology Program of Hunan Province (2014TT2018)
Topics
  • Health Sciences › Medicine › Pharmacology › Apelin-related biomedical research
  • Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
  • Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
Keywords
apelin-13, foam cell formation, autophagy, class III PI3K, Beclin-1, cholesterol efflux, macrophages, lipid accumulation, atherosclerosis, adipokines, cholesterol metabolism
MeSH terms
Beclin-1, Autophagy, Cell Line, Cholesterol, Enzyme Activation, Foam Cells, Humans, Macrophages, Membrane Proteins, Models, Biological, Intercellular Signaling Peptides and Proteins, Atherosclerosis, Lipid Metabolism, Apoptosis Regulatory Proteins, Adipokines, Class III Phosphatidylinositol 3-Kinases

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