Disease Prediction and Drug Development
Arvind Kumar Bansal, Javed Iqbal Khan, S. Kaisar Alam in Introduction to Computational Health Informatics, 2019
Programmed cell-death is the automated death of an inactive cell. There are two types of cell-death: apoptosis and autophagy. Apoptosis occurs due to the lack of survival-factors. Autophagy is a natural degradation that disassembles dysfunctional components. Cytoskeleton gives a cell its shape and facilitates its movement using protein fibers. Extracellular matrix pathways are involved in cell-binding, cell-migration, proliferation and differentiation. The extracellular matrix is made of proteoglycans, water, minerals and fibrous proteins. Proteoglycans have a protein core surrounded by long chains of glycosaminoglycans – a starch like molecule. Angiogenesis is the formation of new blood-vessels. Epigenetic is the heritable changes caused by gene-expression variations with no change in genome sequence.
The Role of Nanoparticles in Cancer Therapy through Apoptosis Induction
Hala Gali-Muhtasib, Racha Chouaib in Nanoparticle Drug Delivery Systems for Cancer Treatment, 2020
Apoptosis is described as type-I programmed cell death, while necrosis typically is known as non-programmed cell death [2]. During apoptosis, the unwanted damaged cells are removed by phagocytosis without leaking their contents into the cytoplasm, and subsequently no inflammatory response occurs. By contrast, necrosis is known as the uncontrolled or unprogrammed type of cell death that is associated with the induction of inflammation [16]. Numerous external stimuli, including specific growth factors, hypoxia radiation and chemotherapeutic drugs, can trigger apoptosis and necrosis. However, not all cells respond similarly to the same stimulus. While certain types of cells may induce apoptosis in response to radiation, other types of cells may undergo necrosis. In addition, the duration and intensity of the stimulus may affect the cell fate. For instance, anti-cancer drugs at lower doses induce apoptosis, but may provoke necrosis at higher doses [16, 17].
Principles of oncology
Professor Sir Norman Williams, Professor P. Ronan O’Connell, Professor Andrew W. McCaskie in Bailey & Love's Short Practice of Surgery, 2018
Apoptosis is a form of programmed cell death which occurs as the direct result of internal cellular events instructing the cell to die. Unlike necrosis, apoptosis is an orderly and internally driven process. The cell dismantles itself neatly for disposal (Figure10.1). There is minimal inflammatory response. Apoptosis is a physiological process. Cells that find themselves in the wrong place normally die by apoptosis and this is an important self-regulatory mechanism in growth and development: cells in the web space of the embryo die by apoptosis, as do lymphocytes that could react to self. The process was rediscovered in 1972, and named apoptosis from the Greek αποπτωσιs, indicating leaf fall. Genes, such as p53, that can activate apoptosis function as tumour suppressor genes. Loss of function in a tumour suppressor gene will contribute to malignant transformation. Cancer cells will be able to evade apoptosis, which means that the wrong cells can be in the wrong places at the wrong times.
The herbicide paraquat-induced molecular mechanisms in the development of acute lung injury and lung fibrosis
Published in Critical Reviews in Toxicology, 2021
Rajasekaran Subbiah, Rajnarayan R. Tiwari
A programmed cell death (apoptosis) is a tightly regulated and highly conserved cell death process during which a damaged or infected or potentially neoplastic cell undergoes self-destruction (Elmore 2007). So, tight regulation of apoptosis is critical for maintaining normal cellular homeostasis. However, deregulated apoptosis has been linked to several pathologies, including chronic inflammation and fibrosis (Favaloro et al. 2012). Many factors, including ROS, DNA damage, and receptor-mediated signals, are reported to activate apoptosis (Solano-Gálvez et al. 2018). Three main signaling pathways mediate programmed cell death. These include an extrinsic pathway involving the interaction of death ligands of the TNF family (TRAIL/Apo2L) with their appropriate cell surface death receptors (TRAIL-R1 (DR4), TRAIL-R2 (DR5), TRAIL-R3 (DcR1), and TRAIL-R4 (DcR1)) or intrinsic pathway involving mitochondria (through Bcl-2 family proteins) or endoplasmic reticulum (ER) stress pathway (Solano-Gálvez et al. 2018).
Protective mechanism of Wnt4 gene on Parkinson’s disease (PD) transgenic Drosophila
Published in International Journal of Neuroscience, 2019
Wei Wu, Yanyin Han, Xiaoli Fan, Qinghua Li, Li Sun
It has become a hot topic to study the pathogenesis of Parkinson's disease from programmed cell death. Programmed cell death includes apoptosis and autophagy, both of which are programmed cell death controlled by related genes, involving the activation, expression and regulation of a series of genes. Autophagy and apoptosis are important physiological mechanisms for recycling multicellular organisms to maintain homeostasis. The occurrence of many neurodegenerative diseases is involved with the dysregulation of autophagy and apoptosis [15], which mainly participates in the recycling and reuse of macromolecule substances and the removal of damaged organelles. It plays an important role in maintaining the homeostasis of the cellular environment and is the main pathway for the degradation of organelles and macromolecule proteins [16].
Assesment of hematotoxic, oxidative and genotoxic damage potentials of fipronil in rainbow trout Oncorhynchus mykiss, Walbaum
Published in Toxicology Mechanisms and Methods, 2021
Arzu Uçar, Veysel Parlak, Aslı Çilingir Yeltekin, Fatma Betül Özgeriş, Özge Çağlar, Hasan Türkez, Gonca Alak, Muhammed Atamanalp
The results showed that 8-OHdG content in the blood tissue of FP treated fish was increased due to dose increase. It is clear that this increase is a response to oxidative damage. Apoptosis is a regular and programmed cell death that occurs in physiological or pathological processes. The mechanism of apoptosis is highly complex and is activated by two major pathways, "extrinsic" and "intrinsic". Both pathways of apoptosis work with caspase (cysteinyl aspartate specific protease) activation. After receiving intrinsic or extrinsic signals, the cells follow the course of caspases mediated pathways. The mitochondria contain cytochrome-c under normal conditions to form ATP. Released cytochrome-c in mitochondrial stress conditions plays an important role in caspase-3 activation in apoptotic cell death (Elmore 2007; Bildik and Bayar 2018). As a final step, caspase-3 activation triggers the activation of cell content proteolysis and DNA fragmentation (Wolf et al. 1999). Therefore, caspase-3 is considered a universal indicator of an apoptotic cell (Ostapchenko et al. 2019). In this study, although Caspase-3 activity increased in blood tissue due to high dose, this change was not statistically significant. The high level of oxidative stress caused by ROS formation stimulates various cell signaling pathways, often associated with apoptosis. Induction of apoptosis by environmental toxicants is associated with a change in the antioxidant defense system leading to oxidative stress in the redox balance. It can be said that this change causes oxidative stress, DNA damage, and apoptosis in fish.
Related Knowledge Centers
- Animal
- Biological Process
- Death
- Necroptosis
- Necrosis
- Autophagy
- Apoptosis
- Cell
- Biological Life Cycle
- BCL-2