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LINK . SPRINGER . COM {}

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We are analyzing https://link.springer.com/article/10.1007/s10495-025-02081-5.

Title:
Cell death signaling in human erythron: erythrocytes lose the complexity of cell death machinery upon maturation | Apoptosis
Description:
Over the recent years, our understanding of the cell death machinery of mature erythrocytes has been greatly expanded. It resulted in the discovery of several regulated cell death (RCD) pathways in red blood cells. Apoptosis (eryptosis) and necroptosis of erythrocytes share certain features with their counterparts in nucleated cells, but they are also critically different in particular details. In this review article, we summarize the cell death subroutines in the erythroid precursors (apoptosis, necroptosis, and ferroptosis) in comparison to mature erythrocytes (eryptosis and erythronecroptosis) to highlight the consequences of organelle clearance and associated loss of multiple components of the cell death machinery upon erythrocyte maturation. Recent advances in understanding the role of erythrocyte RCDs in health and disease have expanded potential clinical applications of these lethal subroutines, emphasizing their contribution to the development of anemia, microthrombosis, and endothelial dysfunction, as well as their role as diagnostic biomarkers and markers of erythrocyte storage-induced lesions. Fas signaling and the functional caspase-8/caspase-3 system are not indispensable for eryptosis, but might be retained in mature erythrocytes to mediate the crosstalk between both erythrocyte-associated RCDs. The ability of erythrocytes to switch between eryptosis and necroptosis suggests that their cell death is not a simple unregulated mechanical disintegration, but a tightly controlled process. This allows investigation of eventual pharmacological interventions aimed at individual cell death subroutines of erythrocytes.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {๐Ÿ“š}

  • Education
  • Telecommunications
  • Science

Content Management System {๐Ÿ“}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {๐Ÿ“ˆ}

What is the average monthly size of link.springer.com audience?

๐ŸŒ  Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 7,542,081 visitors per month in the current month.

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How Does Link.springer.com Make Money? {๐Ÿ’ธ}

We can't see how the site brings in money.

The purpose of some websites isn't monetary gain; they're meant to inform, educate, or foster collaboration. Everyone has unique reasons for building websites. This could be an example. Link.springer.com could have a money-making trick up its sleeve, but it's undetectable for now.

Keywords {๐Ÿ”}

pubmed, cell, google, scholar, article, cas, death, erythrocytes, central, apoptosis, necroptosis, cells, eryptosis, ferroptosis, signaling, erythroid, erythropoiesis, blood, caspase, mature, role, pathways, ros, kinase, regulation, erythrocyte, biol, protein, rcd, machinery, red, apoptotic, stress, differentiation, evidence, mitochondrial, pathway, human, maturation, mitochondria, proteins, activation, clearance, mechanisms, ripk, precursors, studies, mol, multiple, epo,

Topics {โœ’๏ธ}

pro-survival momp-inhibiting bcl-xl tridecylpyrrolidine-diol derivative-induced apoptosis slc38a9โ€“mtor axis-dependent fashion pi3-kinase/akt signaling pathway generated pro-survival p13-tbid jak2/stat5/bcl-xl signalling pro-survival protein bcl-xl ck1ฮฑ-dependent p18-bid phosphorylation ripk1/fadd/caspase-8 necroptosis-regulating necrosome article download pdf tnf-related apoptosis-induced ligand tnf-related apoptosis-inducing ligand redox-sensitive keap1-nrf2 pathway pro-survival anti-apoptotic bcl-2 prevents irradiation-induced myelosuppression functional bcl-xl/bak system prevented myr-p15-tbid bravo-san pedro jm broad-spectrum insect repellent src-family kinase dependency xanthine oxidoreductase-mediated reactions erythroid burst-forming units erythroid colony-forming units burst-forming unit-erythroid colony-forming unit-erythroid ras/raf/mek/erk death receptor-ligand systems pro-inflammatory cytokine-mediated anemia glucose-6-phosphate dehydrogenase deficiency p53/caspase-3 pathway-dependent apoptosis including mitros-mediated ripk1 amyloid ฮฒ-peptide aฮฒ25โ€“35 ripk1/ripk3/mlkl axis bak-derived bh3 peptide fenton chemistry-derived ros ripk1/ripk3/mlkl complex fasl/fadd/caspase-8/caspase-3 axis cytoskeleton-regulating rho gtpases lysosomal-mitochondrial cross-talk jak2/stat5-dependent upregulation ripk1/ripk3-independent manner [151] jak2/stat5-dependent downregulation erythrocyte storage-induced lesions ferreira-da-cruz mde autophagy-related cell death extracellular signal-regulated kinase cell death-promoting inputs death-inducing signaling complex cell type-specific nature represses radiation-induced leukemia

Questions {โ“}

  • Corrons JLV, Casafont LB, Frasnedo EF (2021) Concise review: how do red blood cells born, live, and die?
  • Is the interplay between eryptosis and necroptosis of mature erythrocytes possible?
  • Koonin EV, Krupovic M (2019) Origin of programmed cell death from antiviral defense?
  • Marshall KD, Baines CP (2014) Necroptosis: is there a role for mitochondria?
  • Nemkov T, Reisz JA, Xia Y, Zimring JC, Dโ€™Alessandro A (2018) Red blood cells as an organ?
  • Thiagarajan P, Parker CJ, Prchal JT (2021) How do red blood cells die?
  • Tkachenko A (2024) Hemocompatibility studies in nanotoxicology: hemolysis or eryptosis?
  • What happens to the cell death machinery of erythrocytes upon maturation?
  • Yang WS (2023) Ferroptosis: whERe is the critical site of lipid peroxidation?

Schema {๐Ÿ—บ๏ธ}

WebPage:
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         headline:Cell death signaling in human erythron: erythrocytes lose the complexity of cell death machinery upon maturation
         description:Over the recent years, our understanding of the cell death machinery of mature erythrocytes has been greatly expanded. It resulted in the discovery of several regulated cell death (RCD) pathways in red blood cells. Apoptosis (eryptosis) and necroptosis of erythrocytes share certain features with their counterparts in nucleated cells, but they are also critically different in particular details. In this review article, we summarize the cell death subroutines in the erythroid precursors (apoptosis, necroptosis, and ferroptosis) in comparison to mature erythrocytes (eryptosis and erythronecroptosis) to highlight the consequences of organelle clearance and associated loss of multiple components of the cell death machinery upon erythrocyte maturation. Recent advances in understanding the role of erythrocyte RCDs in health and disease have expanded potential clinical applications of these lethal subroutines, emphasizing their contribution to the development of anemia, microthrombosis, and endothelial dysfunction, as well as their role as diagnostic biomarkers and markers of erythrocyte storage-induced lesions. Fas signaling and the functional caspase-8/caspase-3 system are not indispensable for eryptosis, but might be retained in mature erythrocytes to mediate the crosstalk between both erythrocyte-associated RCDs. The ability of erythrocytes to switch between eryptosis and necroptosis suggests that their cell death is not a simple unregulated mechanical disintegration, but a tightly controlled process. This allows investigation of eventual pharmacological interventions aimed at individual cell death subroutines of erythrocytes.
         datePublished:2025-02-09T00:00:00Z
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      headline:Cell death signaling in human erythron: erythrocytes lose the complexity of cell death machinery upon maturation
      description:Over the recent years, our understanding of the cell death machinery of mature erythrocytes has been greatly expanded. It resulted in the discovery of several regulated cell death (RCD) pathways in red blood cells. Apoptosis (eryptosis) and necroptosis of erythrocytes share certain features with their counterparts in nucleated cells, but they are also critically different in particular details. In this review article, we summarize the cell death subroutines in the erythroid precursors (apoptosis, necroptosis, and ferroptosis) in comparison to mature erythrocytes (eryptosis and erythronecroptosis) to highlight the consequences of organelle clearance and associated loss of multiple components of the cell death machinery upon erythrocyte maturation. Recent advances in understanding the role of erythrocyte RCDs in health and disease have expanded potential clinical applications of these lethal subroutines, emphasizing their contribution to the development of anemia, microthrombosis, and endothelial dysfunction, as well as their role as diagnostic biomarkers and markers of erythrocyte storage-induced lesions. Fas signaling and the functional caspase-8/caspase-3 system are not indispensable for eryptosis, but might be retained in mature erythrocytes to mediate the crosstalk between both erythrocyte-associated RCDs. The ability of erythrocytes to switch between eryptosis and necroptosis suggests that their cell death is not a simple unregulated mechanical disintegration, but a tightly controlled process. This allows investigation of eventual pharmacological interventions aimed at individual cell death subroutines of erythrocytes.
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         Oncology
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         Virology
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               type:PostalAddress
            type:Organization
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      name:First Faculty of Medicine, BIOCEV, Charles University, Vestec, Czech Republic
      name:First Faculty of Medicine, BIOCEV, Charles University, Vestec, Czech Republic
      name:First Department of Medicine โ€“ Hematology, General University Hospital and First Faculty of Medicine, Charles University, Prague, Czech Republic

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