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Updated: Jun 8, 2026
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Biological Compatibility Profile on Biomaterials for Bone Regeneration
Published on: November 16, 2018
[Advances in apoptosis induced by biomaterials]
Keda Wu1, Yuanliang Wang, Jun Pan
1Key Laboratory of Biomechanics & Tissue Engineering under the State Ministry of Education, College of Bioengineering, Chonqing University, Chongqing 400044, China.
Summary
Biomedical materials can induce programmed cell death (apoptosis) through various pathways, including death receptors and mitochondria. Understanding these mechanisms is crucial for developing new biomaterials for disease therapy, particularly cancer treatment.
Area of Science:
- Biomaterials science
- Cell biology
- Molecular biology
Context:
- Biomedical materials are integral to modern medicine, facilitating tissue repair and organ replacement.
- Understanding the molecular-level interactions between biomaterials and biological systems is advancing rapidly.
- Apoptosis, or programmed cell death, plays a vital role in organism development and homeostasis.
Purpose:
- To review the diverse pathways through which biomedical materials can induce apoptosis.
- To explore the mechanisms of biomaterial-induced apoptosis, including signal transduction, reactive oxygen species, and cell adhesion.
- To highlight the significance of this research for biomaterial development and therapeutic applications.
Summary:
- Biomaterial-induced apoptosis involves multiple interconnected pathways, including traditional signal transduction, death receptor pathways, and mitochondrial routes.
- Reactive oxygen species generation and alterations in cell adhesion are also identified as mechanisms by which biomaterials trigger apoptosis.
- The complexity of these pathways underscores the need for in-depth investigation into biomaterial-induced cell death.
Impact:
- This review provides insights into the varied mechanisms of biomaterial-induced apoptosis, crucial for designing effective biomedical materials.
- Understanding these pathways can accelerate the development of novel therapeutic strategies, especially for apoptosis-related diseases like cancer.
- The findings emphasize the potential of biomaterials in advancing disease treatment through controlled induction of cell death.
Related Concept Videos
01:30Apoptosis
Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size reduction of the tissue.
01:24Caspases
Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside cells.
01:17The 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...
01:31The 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...
01:17Phagocytosis 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 by phagocytes.
Normal cells contain receptors that prevent them from being recognized by phagocytes.
01:22Cellular Injury V: Apoptosis and Autophagy
Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...