Unconventional Ways to Live and Die: Cell Death and Survival in Development, Homeostasis, and Disease

Balancing cell death and survival is essential for normal development and homeostasis and for preventing diseases, especially cancer. Conventional cell death pathways include apoptosis, a form of programmed cell death controlled by a well-defined biochemical pathway, and necrosis, the lysis of acutely injured cells. New types of regulated cell death include necroptosis, pyroptosis, ferroptosis, phagoptosis, and entosis. Autophagy can promote survival or can cause death. Newly described processes of anastasis and resuscitation show that, remarkably, cells can recover from the brink of apoptosis or necroptosis. Important new work shows that epithelia achieve homeostasis by extruding excess cells, which then die by anoikis due to loss of survival signals. This mechanically regulated process both maintains barrier function as cells die and matches rates of proliferation and death. In this review, we describe these unconventional ways in which cells have evolved to die or survive, as well as the contributions that these processes make to homeostasis and cancer.

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Proteomic Analysis of Exosomes Released from Heatstressed Hepatocytes Reveals Promotion of Programmed Cell Death Pathways

SSRN Electronic Journal ◽

10.2139/ssrn.3279179 ◽

2018 ◽

Author(s):

Yue Li ◽

Xintao Zhu ◽

Guozhen Wang ◽

Huasheng Tong ◽

Xuguang Ling ◽

...

Keyword(s):

Cell Death ◽

Programmed Cell Death ◽

Proteomic Analysis ◽

Cell Death Pathways

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Implication of ferroptosis in aging

Cell Death Discovery ◽

10.1038/s41420-021-00553-6 ◽

2021 ◽

Vol 7 (1) ◽

Author(s):

Maryam Mazhar ◽

Ahmad Ud Din ◽

Hamid Ali ◽

Guoqiang Yang ◽

Wei Ren ◽

...

Keyword(s):

Cell Death ◽

Neurological Disorders ◽

Accelerated Aging ◽

Underlying Mechanism ◽

Toxic Chemicals ◽

Whole Body ◽

Regulated Cell Death ◽

Age Related ◽

The Subject ◽

Conventional Cell

AbstractLife is indeed continuously going through the irreversible and inevitable process of aging. The rate of aging process depends on various factors and varies individually. These factors include various environmental stimuli including exposure to toxic chemicals, psychological stress whereas suffering with various illnesses specially the chronic diseases serve as endogenous triggers. The basic underlying mechanism for all kinds of stresses is now known to be manifested as production of excessive ROS, exhaustion of ROS neutralizing antioxidant enzymes and proteins leading to imbalance in oxidation and antioxidant processes with subsequent oxidative stress induced inflammation affecting the cells, tissues, organs and the whole body. All these factors lead to conventional cell death either through necrosis, apoptosis, or autophagy. Currently, a newly identified mechanism of iron dependent regulated cell death called ferroptosis, is of special interest for its implication in pathogenesis of various diseases such as cardiovascular disease, neurological disorders, cancers, and various other age-related disorders (ARD). In ferroptosis, the cell death occur neither by conventional apoptosis, necrosis nor by autophagy, rather dysregulated iron in the cell mediates excessive lipid peroxidation of accumulated lethal lipids. It is not surprising to assume its role in aging as previous research have identified some solid cues on the subject. In this review, we will highlight the factual evidences to support the possible role and implication of ferroptosis in aging in order to declare the need to identify and explore the interventions to prevent excessive ferroptosis leading to accelerated aging and associated liabilities of aging.

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The evolution of regulated cell death pathways in animals and their evasion by pathogens

Physiological Reviews ◽

10.1152/physrev.00002.2021 ◽

2022 ◽

Vol 102 (1) ◽

pp. 411-454

Author(s):

Bart Tummers ◽

Douglas R. Green

Keyword(s):

Cell Death ◽

Physiological Traits ◽

Molecular Pathways ◽

Host Pathogen Interactions ◽

Cell Death Pathways ◽

Regulated Cell Death ◽

Host Pathogen ◽

Animal Hosts

The coevolution of host-pathogen interactions underlies many human physiological traits associated with protection from or susceptibility to infections. Among the mechanisms that animals utilize to control infections are the regulated cell death pathways of pyroptosis, apoptosis, and necroptosis. Over the course of evolution these pathways have become intricate and complex, coevolving with microbes that infect animal hosts. Microbes, in turn, have evolved strategies to interfere with the pathways of regulated cell death to avoid eradication by the host. Here, we present an overview of the mechanisms of regulated cell death in Animalia and the strategies devised by pathogens to interfere with these processes. We review the molecular pathways of regulated cell death, their roles in infection, and how they are perturbed by viruses and bacteria, providing insights into the coevolution of host-pathogen interactions and cell death pathways.

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Have necrohormones a role in embryogenesis?

Acta Societatis Botanicorum Poloniae ◽

10.5586/asbp.1996.001 ◽

2014 ◽

Vol 65 (1-2) ◽

pp. 7-9 ◽

Cited By ~ 1

Author(s):

P. R. Bell

Keyword(s):

Cell Death ◽

Somatic Embryogenesis ◽

Programmed Cell Death ◽

Picea Abies ◽

Recent Work ◽

Normal Development ◽

Living Cells ◽

Embryogenic Cultures ◽

Conflicting Evidence ◽

Apomictic Reproduction

The recognition of apoptosis (programmed cell death) as an accompaniment of normal development, the products released by the protoplasts undergoing self-destruction being utilized by adjacent living cells, stimulates renewed interest in Haberlandt's concept of "necrohormones" playing a role in apomictic reproduction. Recent work on somatic embryogenesis in carrot shows that regular death of certain cells in embryogenic cultures satifies the criteria of apoptosis. Similar observations have been made with embryogenic cultures of <em>Picea abies</em>. Haberlandt's claim that cell death induced by injury adjacent to an ovule in <em>Oenothera</em> could lead to parthenogenesis, despite conflicting evidence from later experimenters, is worthy of reexamination.

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Apoptosis in Degenerative Diseases of the Basal Ganglia

The Neuroscientist ◽

10.1177/107385849800400418 ◽

1998 ◽

Vol 4 (4) ◽

pp. 301-311 ◽

Cited By ~ 2

Author(s):

Robert E. Burke

Keyword(s):

Cell Death ◽

Basal Ganglia ◽

Programmed Cell Death ◽

Direct Evidence ◽

Normal Development ◽

Dopamine Neurons ◽

Degenerative Diseases ◽

Morphological Markers ◽

Degenerative Disorders ◽

New Hypothesis

Degenerative disorders of the basal ganglia are characterized by disturbances of motor control. Prototypic examples are Parkinson's disease, which is caused by degeneration of dopamine neurons of the substantia nigra, and Huntington's disease, which is caused by degeneration of neurons of the striatum. In recent years, it has been postulated that some of these disorders may be caused by programmed cell death or apoptosis, a genetically regulated form of cell death. There is clear evidence that apoptosis occurs in neurons of the basal ganglia during normal development, that it can be regulated, and that it can be induced in some animal models of these disorders. Although there is some suggestive direct evidence that apoptosis may occur in the human brain in these disorders, the evidence to date is partial and not yet compelling. Nevertheless, programmed cell death is an important new hypothesis for the pathogenesis of these disorders and warrants vigorous further investigation, particularly with molecular markers in addition to classic morphological markers. The concept of programmed cell death is relevant not only to the pathogenesis of these diseases but also to therapeutic issues, such as transplantation approaches.

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Manipulation of Programmed Cell Death Pathways Enhances Osmotic Stress Tolerance in Plants: Physiological and Molecular Insights

Drought Stress Tolerance in Plants, Vol 1 ◽

10.1007/978-3-319-28899-4_19 ◽

2016 ◽

pp. 439-464 ◽

Cited By ~ 1

Author(s):

Thi My Linh Hoang ◽

Brett Williams ◽

Sagadevan G. Mundree

Keyword(s):

Cell Death ◽

Programmed Cell Death ◽

Osmotic Stress ◽

Stress Tolerance ◽

Cell Death Pathways ◽

Osmotic Stress Tolerance

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Mitochondrial DNA–Related Mitochondrial Dysfunction in Neurodegenerative Diseases

Archives of Pathology & Laboratory Medicine ◽

10.5858/2002-126-0271-mdrmdi ◽

2002 ◽

Vol 126 (3) ◽

pp. 271-280

Author(s):

Russell H. Swerdlow

Keyword(s):

Cell Death ◽

Mitochondrial Dna ◽

Programmed Cell Death ◽

Neurodegenerative Diseases ◽

Mitochondrial Dysfunction ◽

Cell Lines ◽

Late Onset ◽

Cell Death Pathways ◽

Mitochondrial Genotype ◽

Cybrid Cell

Abstract Mitochondrial dysfunction occurs in several late-onset neurodegenerative diseases. Determining its origin and significance may provide insight into the pathogeneses of these disorders. Regarding origin, one hypothesis proposes mitochondrial dysfunction is driven by mitochondrial DNA (mtDNA) aberration. This hypothesis is primarily supported by data from studies of cytoplasmic hybrid (cybrid) cell lines, which facilitate the study of mitochondrial genotype-phenotype relationships. In cybrid cell lines in which mtDNA from persons with certain neurodegenerative diseases is assessed, mitochondrial physiology is altered in ways that are potentially relevant to programmed cell death pathways. Connecting mtDNA-related mitochondrial dysfunction with programmed cell death underscores the crucial if not central role for these organelles in neurodegenerative pathophysiology. This review discusses the cybrid technique and summarizes cybrid data implicating mtDNA-related mitochondrial dysfunction in certain neurodegenerative diseases.

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