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Related Concept Videos

The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

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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...
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The gene encoding the main signaling molecules of the Wnt signaling pathways (the Wnt proteins) was discovered almost four decades ago by Nüsslein-Volhard and Wieschaus. They identified and originally named the gene "wingless" (wg) after a phenotype discovered during their landmark genetic screen in Drosophila for body pattern defects. At around the same time, another researcher named Harold Varmus found that a murine tumor virus activates the mammalian wg homolog, Int-1, which...
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The Extrinsic Apoptotic Pathway01:17

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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...
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Wnt is a zygotic effect gene that is expressed during very early embryonic development. It regulates various processes in animals starting from early development through the adult stage, such as organogenesis in the embryo and maintenance of neuronal and blood stem cells. Wnt proteins can induce a wide variety of intracellular pathways depending upon the specific abilities of different Wnt ligands to form a complex with shared and cognate receptors in the presence of different co-receptors. The...
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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. 
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Related Experiment Video

Updated: May 13, 2025

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis
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Apoptotic vesicles inhibit bone marrow adiposity via wnt/β-catenin signaling.

Yuan Zhu1,2, Yaoshan Liu1, Kunkun Yang1

  • 1Department of Prosthodontics, Peking University School and Hospital of Stomatology, 22 Zhongguancun South Avenue, Beijing 100081, China.

Regenerative Therapy
|April 15, 2025
PubMed
Summary

Apoptotic vesicles (apoVs) reduce bone marrow fat in osteoporosis by activating the Wnt/β-catenin pathway. These apoVs show potential for treating aging-related bone disease, obesity, and other age-related conditions.

Keywords:
Aging-related diseasesApoptotic vesiclesBone marrow adiposityCell-free therapyWnt/β-catenin pathway

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Area of Science:

  • Gerontology
  • Stem Cell Biology
  • Metabolic Diseases

Background:

  • Aging increases osteoporosis incidence and alters bone marrow mesenchymal stem cells (BMMSCs), promoting fat accumulation over bone formation.
  • Reduced osteogenesis and increased adipogenesis in BMMSCs contribute to bone marrow adiposity, a potential therapeutic target for osteoporosis.
  • Apoptotic vesicles (apoVs) are implicated in physiological processes and disease treatment, prompting investigation into their role in bone marrow adiposity.

Purpose of the Study:

  • To investigate the therapeutic potential of BMMSC-derived apoptotic vesicles (apoVs) for treating bone marrow adiposity.
  • To elucidate the specific properties and regulatory mechanisms of apoVs in modulating bone marrow fat accumulation.

Main Methods:

  • Treatment of osteoporotic mice with BMMSC-derived apoVs.
  • Assessment of bone marrow adiposity and adipogenic differentiation in mesenchymal stem cells (MSCs).
  • Analysis of Wnt/β-catenin pathway activation in response to apoV treatment.

Main Results:

  • Apoptotic vesicles (apoVs) significantly decreased bone marrow adiposity in a mouse model of osteoporosis.
  • apoVs inhibited the adipogenic differentiation of MSCs.
  • The therapeutic effect of apoVs was mediated by the activation of the Wnt/β-catenin signaling pathway.

Conclusions:

  • BMMSC-derived apoVs demonstrate efficacy in reducing bone marrow adiposity.
  • apoV-based therapies offer a promising strategy for managing aging-related osteoporosis.
  • These findings suggest potential applications for apoVs in treating obesity and other age-related diseases.