Academia.edu no longer supports Internet Explorer.
To browse Academia.edu and the wider internet faster and more securely, please take a few seconds to upgrade your browser.
1999, The American Journal of Medicine
AI
The article discusses apoptosis as a crucial form of programmed cell death, distinguishing it from necrosis and highlighting its implications in various diseases. It elaborates on the mechanisms of apoptosis, its regulatory processes, and the pathological relevance of alterative apoptotic activities in conditions such as neurodegenerative diseases, autoimmune disorders, and cancers. Emphasizing the dual roles of excessive and deficient apoptosis, the paper underscores the importance of understanding these processes in the context of disease mechanisms to improve therapeutic strategies.
… journal of oncology, 2002
Cell death and the subsequent post-mortem changes, called necrosis, are integral parts of normal development and maturation cycle. Despite the importance of this process, the mechanisms underlying cell death are still poorly understood. In the recent literature, cell death is said to occur by two alternative, opposite modes: apoptosis, a programmed, managed form of cell death, and necrosis, an unordered and accidental form of cellular dying. The incorrect consequence is the overlapping of: a) the process whereby cells die, cell death; and b) the changes that the cells and tissues undergo after the cells die. Only the latter process can be referred to as necrosis and represents a 'no return' process in cell life. In this review, we discuss the excellent basic research developed in this field during last decades and problems that remain to be resolved in defining both experimentally and mechanicistically the events that lead to and characterize cell death. inflammation and disturbed blood supply (1,2). Cell death is an important variable in cancer development, cancer prevention and cancer therapy (3-5). In the treatment of cancer, the major approach is the removal, by surgery, of the neoplasm and/or the induction of cell death in neoplastic cells by radiation, toxic chemicals, antibodies and/or cells of the immune system (6-9). On the other hand, this pathobiological process remains poorly understood and the physiological and biochemical factors that lead to cell death are still not clear. One main factor is the existing confusion between 'apoptosis' process, as compared and contrasted with 'necrosis', leading to the overlapping of the ante mortem changes, i.e. the process of cell death, and the post-mortem changes, i.e. the necrosis process.
This article examines the different characteristics between apoptosis and necrosis, two morphologically distinct manifestations of cell death. Necrosis is non-genetic and triggered by external forces, such as trauma or infection; whereas is apoptosis is a genetically programmed type of cell death. Understanding this difference is not straightforward, yet interpreting the difference is essential for medics in order to deliver the optimal treatment regime. Apoptosis rarely requires medical intervention; however, necrosis always requires medical treatment. Untreated necrosis is dangerous and can lead to death, and it is therefore of considerable medical concern.
Asian Journal of Animal and Veterinary Advances, 2015
The normal cell has its own homeostatic mechanism. A slight deviation in this mechanism leads firstly to an adaptive response in the form of hypertrophy, atrophy etc. But sometimes when adaptive response exceeds a limit also culminates to cell injury which ultimately leads to cell death. Irreversible form of cell injury leads to cell death in the form of necrosis, apoptosis and autophagy and by other alternative ways of necroptosis, anoikis, entosis and cornification. Necrosis and apoptosis are main mechanisms of cell death in mammalian cells. Necrosis is accidental, uncontrolled and un-programmed cell death which leads to cellular swelling, pyknosis, karyolysis, karyorrhexis, disruption of cell membrane and inflammation. Apoptosis is a programmed and energy dependent pathophysiological phenomenon leading to cellular shrinkage but no cell membrane rupture and no inflammatory response. Apoptosis can be mediated by extrinsic, intrinsic and perforin/granzyme pathways, leading to activation of execution caspases and finally protein cleavage, cross linking and DNA-fragmentation. Extrinsic pathway involve ligand (FasL, TNFα) and receptors (FasR, TNFR) interaction which bind to adapter proteins Fas Associated Death Domain (FADD) and TNFα Receptor Associated Death Domain (TRADD) with activation of initiator caspases-8. Intrinsic pathway involves cytochrome c release along with pro-apoptotic proteins and inhibits anti-apoptotic proteins, leads to cytochrome c interaction with Apaf-1, thus activation of pro-caspase-9. Overall, cell death have clarified many aspects of this fundamental process and brought to the attention of scientists its role in a large number of different diseases. The present review describes apoptosis and other alternate mechanisms of cell death with biomedical and veterinary perspectives.
InTech eBooks, 2013
Cell Death and Differentiation, 2010
Current Molecular Medicine, 2008
Apoptosis is a programmed form of cell death with well-defined morphological traits that are often associated with activation of caspases. More recently evidence has become available demonstrating that upon caspase inhibition alternative programs of cell death are executed, including ones with features characteristic of necrosis. These findings have changed our view of necrosis as a passive and essentially accidental form of cell death to that of an active, regulated and controllable process. Also necrosis has now been observed in parallel with, rather than as an alternative pathway to, apoptosis. Thus, cell death responses are extremely flexible despite being programmed. In this review, some of the hallmarks of different programmed cell death modes have been highlighted before focusing the discussion on necrosis. Obligatory events associated with this form of cell death include uncompensated cell swelling and related changes at the plasma membrane. In this context, representatives of the transient receptor channel family and their regulation are discussed. Also mechanisms that lead to execution of the necrotic cell death program are highlighted. Emphasis is laid on summarizing our understanding of events that permit switching between cell death modes and how they connect to necrosis. Finally, potential implications for the treatment of some disease states are mentioned.
IOSR Journal of Pharmacy and Biological Sciences, 2014
Apoptosis is the process of programmed cell death (PCD) which usually occurs in multicellular organisms. In this case, biochemical events leads to morphological cell changes and death. Some of these changes are blebbing, cell shrinkage, nuclear fragmentation, chromatin condensation and chromosomal Deoxyribonucleic Acid (DNA) fragmentation. Apoptosis is however distinct from necrosis which is a form of traumatic cell death that results from acute cellular injury. Apoptosis generally confers advantages during an organism's life cycle. One of the advantages can be seen in the differentiation of fingers and toes in a developing human embryo. This occurs because cells between the fingers apoptose and causes the digits to be separate. Unlike necrosis, apoptosis produces cell fragments called apoptotic bodies that phagocytic cells are able to engulf and quickly remove before the contents of the cell can spill out onto surrounding cells and cause damage. Also, between 50 and 70 billion cells die each day due to apoptosis in the average human adult. For an average child between the ages of 8 and 14, approximately 20 billion to 30 billion cells die a day.. In addition to its importance as a biological phenomenon, defective apoptotic processes have been implicated in an extensive variety of diseases whereby excessive apoptosis causes atrophy and an insufficient apoptosis results in uncontrolled cell proliferation leading to cancer or tumour
Journal of Research and Practice in Dentistry, 2014
Apoptosis is considered as a tightly regulated active process signified by specific morphological and biochemical. On contrary to apoptosis, necrosis is a passive, energy independent pathologic process. The significance of understanding the apoptosis cascade mechanism is imperative as apoptosis being component of both physiological and pathological process. Apoptosis can be stimulated by both physiological and pathological conditions and hence play a role in maintenance of normal homeostasis and in pathogenesis of several diseases. Signaling for apoptosis occurs via caspase dependent and independent pathways that are initiated either from triggering events within the cell or from outside the cell by ligation of death receptors. Present review aims to provide an overview regarding apoptosis, its morphological and biochemical characterstics, its mechanism and its implication in health and diseases.
Methods, 2013
a b s t r a c t 24 Cell death research during the last decades has revealed many molecular signaling cascades, often leading 25 to distinct cell death modalities followed by immune responses. For historical reasons, the prototypic and 26 best characterized cell death modes are apoptosis and necrosis (dubbed necroptosis, to indicate that it is 27 regulated). There is mounting evidence for the interplay between cell death modalities and their redun-28 dant action when one of them is interfered with. This increase in cell death research points to the need for 29 characterizing cell death pathways by different approaches at the biochemical, cellular and if possible, 30 physiological level. In this review we present a selection of techniques to detect cell death and to distin-31 guish necrosis from apoptosis. The distinction should be based on pharmacologic and transgenic 32 approaches in combination with several biochemical and morphological criteria. A particular problem 33 in defining necrosis is that in the absence of phagocytosis, apoptotic cells become secondary necrotic 34 and develop morphologic and biochemical features of primary necrosis.
Undergraduate Journal Club, 2016
Emergency Dermatology, 2009
Bid Cyto c Initiator caspase-9 Endo G AIF Endoplasmic reticulum IP3R ER Stress (misfolded proteins) Plasma Membrane Procaspase-12 TRAF2 Ca ++ Ca ++ Apaf-1 Bcl-2/ Bcl-x L Mitochondria Bcl-2/ Bcl-x L Effector Caspases APOPTOSIS APOPTOSIS APOPTOSIS Effector Caspases Nucleus Initiator Caspase-12 Death domain FIGURE 1.4: The two main pathways for the initiation of apoptosis: the extrinsic pathway and the intrinsic pathway (S. Gupta, A.
Pathology - Research and Practice, 1996
In all normal tissues, cell proliferation and cell death are balanced. The physiology of normal cell death, which has become generally known as apoptosis or programmed cell death, has been intensely investigated in recent years. In this review the cell biology and biochemistry of apoptosis are discussed. Although apoptotic cells can be morphologically recognized, characteristic molecular features such as internucleosomal DNA fragmentation, and histochemical techniques such as in situ end labeling, facilitate the recognition of apoptosis. Many of the genes involved in the regulation of apoptosis, which include cell growth associated genes such as c-myc and p53, have been identified. It has become clear that the bcl-genes (more explicitly bcl-2 and bax) are important apoptosis regulators. The details of the mechanism of programmed cell death are, however, not completely unraveled.
Apoptosis, 2005
We present a comparative study of apoptotic and necrotic morphology (light and scanning electron microscopy), induced by well known experimental conditions (photodynamic treatments, etoposide, hydrogen peroxide, freezing-thawing and serum deprivation) on cell cultures. Our results indicate that morphological criteria (apoptotic cell rounding and shrinkage, and appearance of membrane bubbles in early necrosis) allow to distinguish these cell death mechanisms, and also show that, independently of the damaging agents, the necrotic process occurs in a characteristic sequence (coalescence of membrane bubbles in a single big one that detaches from cells remaining on the substrate).
2019
The balance of cell death and cell formation in multicellular organisms is crucial to maintain proper development, tissue hemostasis and immune regulation. Any dysregulation, at cellular and molecular level, results numerous pathologies. Cell death often evolve as host defense system, in response to pathogens, eliciting inflammation with certain molecular, cellular, biochemical, morphological and physiological changes through various cell death programs. This article reviews major types of cell death (apoptosis, autophagic cell death, necrosis and pyroptosis) as a host defense factor or mediated by inflammation.
International Journal of Livestock Research, 2017
Apoptosis, a Programmed Cell Death (PCD), specifically refers to an energy-dependent, genetically controlled process by which unnecessary or damaged single cells self-destruct when the apoptosis genes are activated. The role of apoptosis in physiology is as significant as that of its counterpart, mitosis. It helps in maintaining cellular homeostasis in the animal body. The number of cells increase or decrease when there is alteration in apoptosis during normal development and aging or during disease. Abnormalities in cell death regulation may cause diseases/conditions. Some conditions are caused due to insufficient apoptosis whereas others due to excessive apoptosis. Presently, large numbers of synthetic and natural compounds have been discovered to be effective against certain diseases through the induction of apoptosis in their target cells.
Loading Preview
Sorry, preview is currently unavailable. You can download the paper by clicking the button above.