scholarly journals Inflammatory caspase regulation: maintaining balance between inflammation and cell death in health and disease

FEBS Journal ◽  
2019 ◽  
Author(s):  
Beatriz E. Bolívar ◽  
Tiphanie P. Vogel ◽  
Lisa Bouchier‐Hayes
Keyword(s):  
Cell Death ◽  
Health And Disease ◽  
Caspase Regulation

scholarly journals The STING1 network regulates autophagy and cell death

2021 ◽  
Vol 6 (1) ◽  
Author(s):  
Ruoxi Zhang ◽  
Rui Kang ◽  
Daolin Tang
Keyword(s):  
Cell Death ◽  
Mitotic Cell ◽  
Therapeutic Interventions ◽  
Type I Interferons ◽  
Microbial Pathogens ◽  
Type I ◽  
Autophagic Degradation ◽  
Health And Disease ◽  
Shed Light ◽  
Pro Inflammatory Cytokines

AbstractCell death and immune response are at the core of life. In past decades, the endoplasmic reticulum (ER) protein STING1 (also known as STING or TMEM173) was found to play a fundamental role in the production of type I interferons (IFNs) and pro-inflammatory cytokines in response to DNA derived from invading microbial pathogens or damaged hosts by activating multiple transcription factors. In addition to this well-known function in infection, inflammation, and immunity, emerging evidence suggests that the STING1-dependent signaling network is implicated in health and disease by regulating autophagic degradation or various cell death modalities (e.g., apoptosis, necroptosis, pyroptosis, ferroptosis, mitotic cell death, and immunogenic cell death [ICD]). Here, we outline the latest advances in our understanding of the regulating mechanisms and signaling pathways of STING1 in autophagy and cell death, which may shed light on new targets for therapeutic interventions.

scholarly journals Ecdysone-induced expression of the caspase DRONC during hormone-dependent programmed cell death in Drosophila is regulated by Broad-Complex

2002 ◽  
Vol 157 (6) ◽  
pp. 985-996 ◽  
Author(s):  
Dimitrios Cakouros ◽  
Tasman Daish ◽  
Damali Martin ◽  
Eric H. Baehrecke ◽  
Sharad Kumar
Keyword(s):  
Gene Expression ◽  
Cell Death ◽  
Steroid Hormone ◽  
Drosophila Cell ◽  
Interaction Sites ◽  
Number Of Genes ◽  
Insect Metamorphosis ◽  
Caspase Regulation ◽  
Broad Complex ◽  
Drosophila Cell Line

The steroid hormone ecdysone regulates both cell differentiation and cell death during insect metamorphosis, by hierarchical transcriptional regulation of a number of genes, including the Broad-Complex (BR-C), the zinc finger family of transcription factors. These genes in turn regulate the transcription of a number of downstream genes. DRONC, a key apical caspase in Drosophila, is the only known caspase that is transcriptionally regulated by ecdysone during development. We demonstrate that dronc gene expression is ablated or reduced in BR-C mutant flies. Using RNA interference in an ecdysone-responsive Drosophila cell line, we show that DRONC is essential for ecdysone-mediated cell death, and that dronc upregulation in these cells is controlled by BR-C. Finally, we show that the dronc promoter has BR-C interaction sites, and that it can be transactivated by a specific isoform of BR-C. These results indicate that BR-C plays a key role in ecdysone-mediated caspase regulation.

scholarly journals Involvement of Src in the Adaptation of Cancer Cells under Microenvironmental Stresses

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
A. K. M. Mahbub Hasan ◽  
Takashi Ijiri ◽  
Ken-ichi Sato
Keyword(s):  
Cell Death ◽  
Cancer Cells ◽  
Tyrosine Phosphorylation ◽  
Protein Tyrosine Kinase ◽  
Protein Tyrosine Phosphorylation ◽  
Cellular Functions ◽  
Specific Behavior ◽  
Protein Tyrosine ◽  
Health And Disease ◽  
The Relationship

Protein-tyrosine phosphorylation, which is catalyzed by protein-tyrosine kinase (PTK), plays a pivotal role in a variety of cellular functions related to health and disease. The discovery of the viral oncogene Src (v-Src) and its cellular nontransforming counterpart (c-Src), as the first example of PTK, has opened a window to study the relationship between protein-tyrosine phosphorylation and the biology and medicine of cancer. In this paper, we focus on the roles played by Src and other PTKs in cancer cell-specific behavior, that is, evasion of apoptosis or cell death under stressful extracellular and/or intracellular microenvironments (i.e., hypoxia, anoikis, hypoglycemia, and serum deprivation).

Caspase regulation of genotoxin-induced neural precursor cell death

2003 ◽  
Vol 74 (3) ◽  
pp. 435-445 ◽  
Author(s):  
Cleta D'Sa ◽  
Barbara J. Klocke ◽  
Francesco Cecconi ◽  
Tulia Lindsten ◽  
Craig B. Thompson ◽  
...  
Keyword(s):  
Cell Death ◽  
Precursor Cell ◽  
Neural Precursor ◽  
Neural Precursor Cell ◽  
Caspase Regulation

scholarly journals An Overview of Iron Metabolism in Health and Disease

2021 ◽  
pp. 70-78
Author(s):  
Nabiyev Abdusamat Utkurovich
Keyword(s):  
Cell Death ◽  
Iron Metabolism ◽  
Growth And Development ◽  
Biochemical Parameters ◽  
Cellular Level ◽  
The Body ◽  
Viral Diseases ◽  
Correct Interpretation ◽  
Working Capacity ◽  
Health And Disease

Human iron metabolism is the set of chemical reactions that maintain human homeostasis of iron at the systemic and cellular level. Iron is both necessary to the body and potentially toxic. Controlling iron levels in the body is a critically important part of many aspects of human health and disease. Iron deficiency states are the reason for a decrease in working capacity, an increase in susceptibility to viral diseases, especially in children and cause growth and development retardation. Iron overload and poisoning lead to the activation of processes that can cause cell death. Timely diagnosis of disorders of iron metabolism and subsequent monitoring of treatment require knowledge of not only pathophysiological mechanisms, but also methodological capabilities and correct interpretation of clinical and biochemical parameters of iron metabolism.

scholarly journals Enzymatically oxidized phospholipids assume center stage as essential regulators of innate immunity and cell death

2019 ◽  
Vol 12 (574) ◽  
pp. eaau2293 ◽  
Author(s):  
Valerie B. O’Donnell ◽  
Maceler Aldrovandi ◽  
Robert C. Murphy ◽  
Gerhard Krönke
Keyword(s):  
Cardiovascular Disease ◽  
Cell Death ◽  
Immune Cells ◽  
Blood Clotting ◽  
Biosynthetic Pathways ◽  
Oxidized Phospholipids ◽  
Center Stage ◽  
Cellular Events ◽  
Health And Disease ◽  
Enzymatic Pathways

Enzymatically oxidized phospholipids (eoxPLs) are formed through regulated processes by which eicosanoids or prostaglandins are attached to phospholipids (PLs) in immune cells. These eoxPLs comprise structurally diverse families of biomolecules with potent bioactivities, and they have important immunoregulatory roles in both health and disease. The formation of oxPLs through enzymatic pathways and their signaling capabilities are emerging concepts. This paradigm is changing our understanding of eicosanoid, prostaglandin, and PL biology in health and disease. eoxPLs have roles in cellular events such as ferroptosis, apoptosis, and blood clotting and diseases such as arthritis, diabetes, and cardiovascular disease. They are increasingly recognized as endogenous bioactive mediators and potential targets for drug development. This review will describe recent evidence that places eoxPLs and their biosynthetic pathways center stage in immunoregulation.

scholarly journals Ferroptosis in infection, inflammation, and immunity

2021 ◽  
Vol 218 (6) ◽  
Author(s):  
Xin Chen ◽  
Rui Kang ◽  
Guido Kroemer ◽  
Daolin Tang
Keyword(s):  
Cell Death ◽  
Membrane Damage ◽  
Iron Toxicity ◽  
Innate And Adaptive Immunity ◽  
Plasma Membrane Damage ◽  
Novel Treatment ◽  
Regulated Necrosis ◽  
Health And Disease ◽  
Enzymatic Pathways ◽  
Disease Understanding

Ferroptosis is a type of regulated necrosis that is triggered by a combination of iron toxicity, lipid peroxidation, and plasma membrane damage. The upstream inducers of ferroptosis can be divided into two categories (biological versus chemical) and activate two major pathways (the extrinsic/transporter versus the intrinsic/enzymatic pathways). Excessive or deficient ferroptotic cell death is implicated in a growing list of physiological and pathophysiological processes, coupled to a dysregulated immune response. This review focuses on new discoveries related to how ferroptotic cells and their spilled contents shape innate and adaptive immunity in health and disease. Understanding the immunological characteristics and activity of ferroptotic death not only illuminates an intersection between cell death and immunity but may also lead to the development of novel treatment approaches for immunopathological diseases.

scholarly journals The NF-κB-mediated control of the JNK cascade in the antagonism of programmed cell death in health and disease

2006 ◽  
Vol 13 (5) ◽  
pp. 712-729 ◽  
Author(s):  
S Papa ◽  
C Bubici ◽  
F Zazzeroni ◽  
C G Pham ◽  
C Kuntzen ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Health And Disease ◽  
Jnk Cascade

scholarly journals The Role of Mitophagy in Regulating Cell Death

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Sunao Li ◽  
Jiaxin Zhang ◽  
Chao Liu ◽  
Qianliang Wang ◽  
Jun Yan ◽  
...  
Keyword(s):  
Cell Death ◽  
Cytosolic Calcium ◽  
Cellular Functions ◽  
Power Generators ◽  
Unfolded Protein ◽  
Mitochondrial Homeostasis ◽  
Cell Death Pathways ◽  
Health And Disease ◽  
Protein Response

Mitochondria are multifaceted organelles that serve to power critical cellular functions, including act as power generators of the cell, buffer cytosolic calcium overload, production of reactive oxygen species, and modulating cell survival. The structure and the cellular location of mitochondria are critical for their function and depend on highly regulated activities such as mitochondrial quality control (MQC) mechanisms. The MQC is regulated by several sets of processes: mitochondrial biogenesis, mitochondrial fusion and fission, mitophagy, and other mitochondrial proteostasis mechanisms such as mitochondrial unfolded protein response (mtUPR) or mitochondrial-derived vesicles (MDVs). These processes are important for the maintenance of mitochondrial homeostasis, and alterations in the mitochondrial function and signaling are known to contribute to the dysregulation of cell death pathways. Recent studies have uncovered regulatory mechanisms that control the activity of the key components for mitophagy. In this review, we discuss how mitophagy is controlled and how mitophagy impinges on health and disease through regulating cell death.

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