Related Experiment Video

Updated: Apr 3, 2026

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
07:15

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Published on: August 23, 2024

1.1K

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

Feng Yao1, Yun-Cheng Lv2, Min Zhang2

  • 1Institute of Cardiovascular Research, Key Laboratory for Atherosclerology of Hunan Province, University of South China, Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, Hengyang 421001, Hunan, China; Department of Laboratory Animal Science, University of South China, Hengyang 421001, Hunan, China.

Biochemical and Biophysical Research Communications
|September 20, 2015
PubMed

Insights

Apelin-13 reduces lipid accumulation in macrophages by enhancing cholesterol efflux and inducing autophagy through the Class III PI3K/Beclin-1 pathway, offering a new therapeutic strategy for atherosclerosis.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Cardiovascular Research

Background:

  • Apelin-13, an adipokine, facilitates cholesterol efflux in macrophages, exhibiting antiatherosclerotic properties.
  • Autophagy, a cellular stress response, plays a role in the development of atherosclerosis.

Purpose of the Study:

  • To investigate if apelin-13 regulates cholesterol metabolism in macrophage foam cells via autophagy.
  • To elucidate the underlying molecular mechanisms involved in this process.

Main Methods:

  • Utilized THP-1 derived macrophages to assess lipid accumulation and cholesterol efflux.
  • Investigated the role of Class III phosphoinositide 3-kinase (PI3K) and Beclin-1 in apelin-13-induced autophagy.
  • Employed inhibition of Class III PI3K and Beclin-1 to confirm their involvement.

Main Results:

  • Apelin-13 significantly reduced lipid accumulation in macrophages by enhancing cholesterol efflux.
  • Apelin-13 treatment induced autophagy, evidenced by the activation of Class III PI3K and Beclin-1.
  • Inhibiting Class III PI3K or Beclin-1 attenuated the effects of apelin-13 on autophagy.

Conclusions:

  • Apelin-13 diminishes foam cell lipid accumulation by activating autophagy through the Class III PI3K/Beclin-1 pathway.
  • This study provides novel insights into apelin-13's role in inhibiting foam cell formation.
  • Autophagy emerges as a potential therapeutic target for treating atherosclerosis.
Keywords:
Apelin-13AutophagyCholesterol effluxClass III PI3K/Beclin-1Macrophage foam cells

More Related Videos

Identification of Mediators of T-cell Receptor Signaling via the Screening of Chemical Inhibitor Libraries08:49

Identification of Mediators of T-cell Receptor Signaling via the Screening of Chemical Inhibitor Libraries

Published on: January 22, 2019

9.7K
Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death09:18

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

Published on: December 27, 2016

9.2K

Related Concept Videos

The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
9.2K
Phagocytosis of Apoptotic Cells01:17

Phagocytosis of Apoptotic Cells

Cells undergoing apoptosis form apoptotic bodies that must be removed immediately to prevent inflammation, autoimmune diseases, and necrosis. Phagocytosis is carried out by professional phagocytes such as macrophages or  immature dendritic cells. Non-professional phagocytes such as  epithelial cells and fibroblasts also take part in this process; however, they are not as effective as professional phagocytes. 
Normal cells contain receptors that prevent them from being recognized...
5.6K
Mechanism of Filopodia Formation01:39

Mechanism of Filopodia Formation

Filopodia are thin, actin-rich cellular protrusions that play an important role in many fundamental cellular functions. They vary in their occurrence, length, and positioning in different cell types, suggesting their diverse roles.
Their main function is to guide migrating cells during normal tissue morphogenesis or cancer metastasis by recognizing and making initial contacts with the extracellular matrix. However, they can also act as stationary cell anchors or help to establish communication...
3.4K
Role of Ephrin-Eph Signalling in Intestinal Stem Cell Renewal01:22

Role of Ephrin-Eph Signalling in Intestinal Stem Cell Renewal

Erythropoietin-producing hepatocellular carcinoma receptor (Eph) and its ligand, Eph receptor-interacting protein (Ephrin) were first discovered in the human carcinoma cell line, hence the name. Ephrin-Eph interaction guides cells to reach their appropriate location in adult tissues. They also play an essential role in the immune system by helping in immune cell migration, adhesion, and activation. Based on their structure and function, Eph is divided into two classes — EphA and EphB.
2.8K
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
6.4K
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
9.3K