-
Toxicologic Pathology Jun 2007The process of programmed cell death, or apoptosis, is generally characterized by distinct morphological characteristics and energy-dependent biochemical mechanisms.... (Review)
Review
The process of programmed cell death, or apoptosis, is generally characterized by distinct morphological characteristics and energy-dependent biochemical mechanisms. Apoptosis is considered a vital component of various processes including normal cell turnover, proper development and functioning of the immune system, hormone-dependent atrophy, embryonic development and chemical-induced cell death. Inappropriate apoptosis (either too little or too much) is a factor in many human conditions including neurodegenerative diseases, ischemic damage, autoimmune disorders and many types of cancer. The ability to modulate the life or death of a cell is recognized for its immense therapeutic potential. Therefore, research continues to focus on the elucidation and analysis of the cell cycle machinery and signaling pathways that control cell cycle arrest and apoptosis. To that end, the field of apoptosis research has been moving forward at an alarmingly rapid rate. Although many of the key apoptotic proteins have been identified, the molecular mechanisms of action or inaction of these proteins remain to be elucidated. The goal of this review is to provide a general overview of current knowledge on the process of apoptosis including morphology, biochemistry, the role of apoptosis in health and disease, detection methods, as well as a discussion of potential alternative forms of apoptosis.
Topics: Animals; Apoptosis; DNA Fragmentation; Humans; Necrosis
PubMed: 17562483
DOI: 10.1080/01926230701320337 -
Aging Apr 2016Apoptosis is a form of programmed cell death that results in the orderly and efficient removal of damaged cells, such as those resulting from DNA damage or during... (Review)
Review
Apoptosis is a form of programmed cell death that results in the orderly and efficient removal of damaged cells, such as those resulting from DNA damage or during development. Apoptosis can be triggered by signals from within the cell, such as genotoxic stress, or by extrinsic signals, such as the binding of ligands to cell surface death receptors. Deregulation in apoptotic cell death machinery is an hallmark of cancer. Apoptosis alteration is responsible not only for tumor development and progression but also for tumor resistance to therapies. Most anticancer drugs currently used in clinical oncology exploit the intact apoptotic signaling pathways to trigger cancer cell death. Thus, defects in the death pathways may result in drug resistance so limiting the efficacy of therapies. Therefore, a better understanding of the apoptotic cell death signaling pathways may improve the efficacy of cancer therapy and bypass resistance. This review will highlight the role of the fundamental regulators of apoptosis and how their deregulation, including activation of anti-apoptotic factors (i.e., Bcl-2, Bcl-xL, etc) or inactivation of pro-apoptotic factors (i.e., p53 pathway) ends up in cancer cell resistance to therapies. In addition, therapeutic strategies aimed at modulating apoptotic activity are briefly discussed.
Topics: Animals; Antineoplastic Agents; Apoptosis; Disease Progression; Humans; Neoplasms; Signal Transduction
PubMed: 27019364
DOI: 10.18632/aging.100934 -
Annals of Allergy, Asthma & Immunology... Mar 1997Reading this article will introduce the reader to the basic concept of physiologic cell death referred to as apoptosis. In addition, the role of apoptosis in immune... (Review)
Review
LEARNING OBJECTIVES
Reading this article will introduce the reader to the basic concept of physiologic cell death referred to as apoptosis. In addition, the role of apoptosis in immune function as well as its contribution to various clinical disorders will be developed.
DATA SOURCE
The author's experience with recently described patients who have a unique autoimmune syndrome associated with a defect in apoptosis. In addition, recent reviews on the subject of apoptosis in health and disease served as informational outlines.
STUDY SELECTION
Data source included pertinent reviews and articles meeting the educational objectives and these were critically reviewed.
RESULTS
Apoptosis is a critical process in cellular homeostasis that only recently has been appreciated. Its role in both immune development and the control of immune responses as well as in T cell cytotoxic effector function has been established. Information is accumulating that diseases such as cancer can be linked to underlying defects in the apoptosis pathway allowing cells that normally would have been eliminated to live. The role of alterations in apoptosis in other chronic diseases, including autoimmune and neurodegenerative disorders, is beginning to emerge.
CONCLUSIONS
Apoptosis plays a central part in normal tissue homeostasis as well as having a role in a variety of clinical diseases that are characterized by either increased or decreased cell survival.
Topics: Apoptosis; Humans
PubMed: 9087147
DOI: 10.1016/S1081-1206(10)63176-6 -
Seminars in Immunology Nov 2023Neutrophils are among the most abundant immune cells, representing about 50%- 70% of all circulating leukocytes in humans. Neutrophils rapidly infiltrate inflamed... (Review)
Review
Neutrophils are among the most abundant immune cells, representing about 50%- 70% of all circulating leukocytes in humans. Neutrophils rapidly infiltrate inflamed tissues and play an essential role in host defense against infections. They exert microbicidal activity through a variety of specialized effector mechanisms, including phagocytosis, production of reactive oxygen species, degranulation and release of secretory vesicles containing broad-spectrum antimicrobial factors. In addition to their homeostatic turnover by apoptosis, recent studies have revealed the mechanisms by which neutrophils undergo various forms of regulated cell death. In this review, we will discuss the different modes of regulated cell death that have been described in neutrophils, with a particular emphasis on the current understanding of neutrophil pyroptosis and its role in infections and autoinflammation.
Topics: Humans; Neutrophils; Pyroptosis; Phagocytosis; Apoptosis
PubMed: 37939552
DOI: 10.1016/j.smim.2023.101849 -
Journal of Pineal Research Oct 2015Endoplasmic reticulum (ER) is a dynamic organelle that participates in a number of cellular functions by controlling lipid metabolism, calcium stores, and proteostasis.... (Review)
Review
Endoplasmic reticulum (ER) is a dynamic organelle that participates in a number of cellular functions by controlling lipid metabolism, calcium stores, and proteostasis. Under stressful situations, the ER environment is compromised, and protein maturation is impaired; this causes misfolded proteins to accumulate and a characteristic stress response named unfolded protein response (UPR). UPR protects cells from stress and contributes to cellular homeostasis re-establishment; however, during prolonged ER stress, UPR activation promotes cell death. ER stressors can modulate autophagy which in turn, depending of the situation, induces cell survival or death. Interactions of different autophagy- and apoptosis-related proteins and also common signaling pathways have been found, suggesting an interplay between these cellular processes, although their dynamic features are still unknown. A number of pathologies including metabolic, neurodegenerative and cardiovascular diseases, cancer, inflammation, and viral infections are associated with ER stress, leading to a growing interest in targeting components of the UPR as a therapeutic strategy. Melatonin has a variety of antioxidant, anti-inflammatory, and antitumor effects. As such, it modulates apoptosis and autophagy in cancer cells, neurodegeneration and the development of liver diseases as well as other pathologies. Here, we review the effects of melatonin on the main ER stress mechanisms, focusing on its ability to regulate the autophagic and apoptotic processes. As the number of studies that have analyzed ER stress modulation by this indole remains limited, further research is necessary for a better understanding of the crosstalk between ER stress, autophagy, and apoptosis and to clearly delineate the mechanisms by which melatonin modulates these responses.
Topics: Animals; Apoptosis; Autophagy; Endoplasmic Reticulum Stress; Humans; Melatonin
PubMed: 26201382
DOI: 10.1111/jpi.12264 -
Archives of Biochemistry and Biophysics Jan 2022Vascular endothelial cells (VECs), which are lined up in the inner surface of blood vessels, are in direct contact with the metabolite-related endogenous danger signals... (Review)
Review
Vascular endothelial cells (VECs), which are lined up in the inner surface of blood vessels, are in direct contact with the metabolite-related endogenous danger signals in the circulatory system. Moreover, VECs death impairs vasodilation and increases endothelium-dependent permeability, which is strongly correlated with the development of atherosclerosis (AS). Among several forms of cell death, regulatory death of endothelial cells frequently occurs in AS, mainly including ferroptosis, pyroptosis, apoptosis and autophagy. In this review, we summarize regulatory factors and signaling mechanisms of regulatory death in endothelial cells, discussing their effects in the context of the atherosclerotic procession.
Topics: Animals; Apoptosis; Atherosclerosis; Autophagy; Endothelial Cells; Ferroptosis; Humans; Pyroptosis
PubMed: 34856194
DOI: 10.1016/j.abb.2021.109098 -
Advances in Genetics 1997
Review
Topics: Animals; Apoptosis; Humans; Ischemia; Liver; Microscopy, Electron; Models, Biological; Necrosis; Neoplasms
PubMed: 9348645
DOI: 10.1016/s0065-2660(08)60447-2 -
Frontiers in Bioscience : a Journal and... May 2007Apoptosis plays a critical role in maintaining tissue homeostasis and represents a normal function to eliminate excess or dysfunctional cells. Accumulated evidence... (Review)
Review
Apoptosis plays a critical role in maintaining tissue homeostasis and represents a normal function to eliminate excess or dysfunctional cells. Accumulated evidence suggest that apoptosis helps to maintain cellular homeostasis during the menstrual cycle by eliminating senescent cells from the functional layer of the uterine endometrium during the late secretory and menstrual phase of the cycle. BCL-2 family and Fas/FasL system have been extensively studied in human endometrium and endometriotic tissues. Eutopic endometrium from women with endometriosis reportedly has some fundamental differences compared with normal endometrium of women without endometriosis. The differences could contribute to the survival of regurgitating endometrial cells into the peritoneal cavity and the development of endometriosis. One mechanism that recently gained a lot of interest is the finding that apoptosis appeared in eutopic and ectopic endometrium of patients with endometriosis. This study is a current review of the literature focused on the physiological role of apoptosis in normal endometrium and the alterations in regulation of apoptosis in eutopic and ectopic endometrium from women with endometriosis. Finally, role of apoptosis in the treatment of endometriosis is reviewed to link the basic research findings into clinical applications.
Topics: Apoptosis; Endometriosis; Endometrium; Female; Humans
PubMed: 17485289
DOI: 10.2741/2302 -
Annals of Neurology Dec 1995Apoptosis is a mode of cell death in which the cell plays an active role in its own demise. The study of neural apoptosis, the identification of genes controlling... (Review)
Review
Apoptosis is a mode of cell death in which the cell plays an active role in its own demise. The study of neural apoptosis, the identification of genes controlling apoptosis, and the examination of the mechanisms by which these genes achieve their effects have assumed increasing importance over the past few years. This is because (1) neural apoptosis occurs not only in development, but also in pathophysiological states such as stroke, glutamate toxicity, and beta-amyloid peptide toxicity; (2) genes that control apoptotic cell death, such as bcl-2, p35, p53, and p75NTR, also modulate necrotic neural death in some cases; (3) the emerging mechanisms by which these genes control apoptosis may be relevant for understanding neurodegenerative processes, and for the design of therapeutic agents; and (4) the findings that the cell plays an active role in its own demise, and that specific gene products are involved, suggest that therapeutic intervention may be feasible.
Topics: Animals; Apoptosis; Humans; Neurons
PubMed: 8526456
DOI: 10.1002/ana.410380604 -
Protein and Peptide Letters 2021Apoptosis, also named programmed cell death, is a highly conserved physiological mechanism. Apoptosis plays crucial roles in many life processes, such as tissue... (Review)
Review
Apoptosis, also named programmed cell death, is a highly conserved physiological mechanism. Apoptosis plays crucial roles in many life processes, such as tissue development, organ formation, homeostasis maintenance, resistance against external aggression, and immune responses. Apoptosis is regulated by many genes, among which Apoptosis Inhibitor-5 (API5) is an effective inhibitor, though the structure of API5 is completely different from the other known Inhibitors of Apoptosis Proteins (IAPs). Due to its high expression in many types of tumors, API5 has received extensive attention, and may be an effective target for cancer treatment. In order to comprehensively and systematically understand the biological roles of API5, we summarized the evolution and structure of API5 and its roles in anti-apoptosis in this review.
Topics: Animals; Apoptosis; Apoptosis Regulatory Proteins; Humans; Mice; Models, Molecular; Nuclear Proteins; Protein Conformation; Rats
PubMed: 33319655
DOI: 10.2174/0929866527999201211195551