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  1. Article ; Online: Cell Death Pathways Drive Necroinflammation during Acute Kidney Injury.

    von Mässenhausen, Anne / Tonnus, Wulf / Linkermann, Andreas

    Nephron

    2018  Volume 140, Issue 2, Page(s) 144–147

    Abstract: Renal tubules represent an intercellular unit and function as a syncytium. When acute tubular necrosis was first visualized to occur through a process of synchronized regulated necrosis (SRN) in handpicked primary renal tubules, it became obvious that ... ...

    Abstract Renal tubules represent an intercellular unit and function as a syncytium. When acute tubular necrosis was first visualized to occur through a process of synchronized regulated necrosis (SRN) in handpicked primary renal tubules, it became obvious that SRN actually promotes nephron loss. This realization adds to our current understanding of acute kidney injury (AKI)-chronic kidney disease (CKD) transition and argues for the prevention of AKI episodes to prevent CKD progression. Because SRN is triggered by necroptosis and executed by ferroptosis, 2 recently identified signaling pathways of regulated necrosis, a combination therapy employing necrostatins and ferrostatins may be beneficial for protection against nephron loss. Clinical trials in AKI and during the process of kidney transplantation are now required to prevent SRN. Additionally, necrotic cell death drives autoimmunity and necroinflammation and therefore represents a therapeutic target even for the prevention of antibody-mediated rejection of allografts years after the transplantation process.
    MeSH term(s) Acute Kidney Injury/pathology ; Apoptosis ; Cell Death ; Disease Progression ; Humans ; Kidney/pathology ; Necrosis ; Nephritis/pathology
    Language English
    Publishing date 2018-06-29
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 207121-6
    ISSN 2235-3186 ; 1423-0186 ; 1660-8151 ; 0028-2766
    ISSN (online) 2235-3186 ; 1423-0186
    ISSN 1660-8151 ; 0028-2766
    DOI 10.1159/000490807
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 169: Show issues Location:
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    ab Jg. 2022: Lesesaal (EG)

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  2. Article ; Online: Rubicon-deficiency sensitizes mice to mixed lineage kinase domain-like (MLKL)-mediated kidney ischemia-reperfusion injury.

    Tonnus, Wulf / Locke, Sophie / Meyer, Claudia / Maremonti, Francesca / Eggert, Lena / von Mässenhausen, Anne / Bornstein, Stefan R / Green, Douglas R / Linkermann, Andreas

    Cell death & disease

    2022  Volume 13, Issue 3, Page(s) 236

    Abstract: The cytosolic protein rubicon (RUBCN) has been implicated in the removal of necrotic debris and autoimmunity. However, the role of RUBCN in models of acute kidney injury (AKI), a condition that typically involves necrotic kidney tubules, was not ... ...

    Abstract The cytosolic protein rubicon (RUBCN) has been implicated in the removal of necrotic debris and autoimmunity. However, the role of RUBCN in models of acute kidney injury (AKI), a condition that typically involves necrotic kidney tubules, was not investigated. Here, we demonstrate that RUBCN-deficient mice are hypersensitive to renal damage induced by ischemia-reperfusion injury (IRI) and cisplatin-induced AKI. Combined deficiency of RUBCN and mixed lineage kinase domain-like (MLKL) partially reversed the sensitivity in the IRI model suggesting that the absence of RUBCN sensitizes to necroptosis in that model. Necroptosis is known to contribute to TNFα-induced severe inflammatory response syndrome (SIRS), but we detected no statistically significant difference in overall survival following injection of TNFα in RUBCN-deficient mice. We additionally generated RUBCN-deficient mice which lack gasdermin D (GSDMD), the terminal mediator of pyroptosis, but no reversal of the AKI phenotype was observed. Finally, and in contrast to the previous understanding of the role of RUBCN, we did not find a significant autoimmune phenotype in RUBCN-deficient mice, but detected chronic kidney injury (CKD) in aged RUBCN-deficient mice of both sexes. In summary, our data indicate that RUBCN-deficient mice are hypersensitive to kidney injury.
    MeSH term(s) Acute Kidney Injury/chemically induced ; Acute Kidney Injury/genetics ; Animals ; Female ; Intracellular Signaling Peptides and Proteins/metabolism ; Kidney/metabolism ; Kidney Tubules/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Protein Kinases/metabolism ; Receptor-Interacting Protein Serine-Threonine Kinases/metabolism ; Reperfusion Injury/genetics ; Reperfusion Injury/metabolism ; Tumor Necrosis Factor-alpha/metabolism
    Chemical Substances Intracellular Signaling Peptides and Proteins ; Rubcn protein, mouse ; Tumor Necrosis Factor-alpha ; MLKL protein, mouse (EC 2.7.-) ; Protein Kinases (EC 2.7.-) ; Receptor-Interacting Protein Serine-Threonine Kinases (EC 2.7.11.1)
    Language English
    Publishing date 2022-03-14
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2541626-1
    ISSN 2041-4889 ; 2041-4889
    ISSN (online) 2041-4889
    ISSN 2041-4889
    DOI 10.1038/s41419-022-04682-3
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  3. Article ; Online: Treatment with siRNAs is commonly associated with GPX4 up-regulation and target knockdown-independent sensitization to ferroptosis.

    von Mässenhausen, Anne / Schlecht, Marlena Nastassja / Beer, Kristina / Maremonti, Francesca / Tonnus, Wulf / Belavgeni, Alexia / Gavali, Shubhangi / Flade, Karolin / Riley, Joel S / Zamora Gonzalez, Nadia / Brucker, Anne / Becker, Jorunn Naila / Tmava, Mirela / Meyer, Claudia / Peitzsch, Mirko / Hugo, Christian / Gembardt, Florian / Angeli, Jose Pedro Friedmann / Bornstein, Stefan R /
    Tait, Stephen W G / Linkermann, Andreas

    Science advances

    2024  Volume 10, Issue 11, Page(s) eadk7329

    Abstract: Small interfering RNAs (siRNAs) are widely used in biomedical research and in clinical trials. Here, we demonstrate that siRNA treatment is commonly associated with significant sensitization to ferroptosis, independently of the target protein knockdown. ... ...

    Abstract Small interfering RNAs (siRNAs) are widely used in biomedical research and in clinical trials. Here, we demonstrate that siRNA treatment is commonly associated with significant sensitization to ferroptosis, independently of the target protein knockdown. Genetically targeting mitochondrial antiviral-signaling protein (MAVS) reversed the siRNA-mediated sensitizing effect, but no activation of canonical MAVS signaling, which involves phosphorylation of IkBα and interferon regulatory transcription factor 3 (IRF3), was observed. In contrast, MAVS mediated a noncanonical signal resulting in a prominent increase in mitochondrial ROS levels, and increase in the BACH1/pNRF2 transcription factor ratio and GPX4 up-regulation, which was associated with a 50% decrease in intracellular glutathione levels. We conclude that siRNAs commonly sensitize to ferroptosis and may severely compromise the conclusions drawn from silencing approaches in biomedical research. Finally, as ferroptosis contributes to a variety of pathophysiological processes, we cannot exclude side effects in human siRNA-based therapeutical concepts that should be clinically tested.
    MeSH term(s) Humans ; Signal Transduction ; RNA, Small Interfering/genetics ; Ferroptosis/genetics ; Up-Regulation ; Transcription Factors/metabolism
    Chemical Substances RNA, Small Interfering ; Transcription Factors
    Language English
    Publishing date 2024-03-15
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2810933-8
    ISSN 2375-2548 ; 2375-2548
    ISSN (online) 2375-2548
    ISSN 2375-2548
    DOI 10.1126/sciadv.adk7329
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  4. Article ; Online: Induction of ferroptosis selectively eliminates senescent tubular cells.

    Liao, Chieh M / Wulfmeyer, Vera C / Chen, Rongjun / Erlangga, Zulrahman / Sinning, Julius / von Mässenhausen, Anne / Sörensen-Zender, Inga / Beer, Kristina / von Vietinghoff, Sibylle / Haller, Hermann / Linkermann, Andreas / Melk, Anette / Schmitt, Roland

    American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons

    2022  Volume 22, Issue 9, Page(s) 2158–2168

    Abstract: The accumulation of senescent cells is an important contributor to kidney aging, chronic renal disease, and poor outcome after kidney transplantation. Approaches to eliminate senescent cells with senolytic compounds have been proposed as novel strategies ...

    Abstract The accumulation of senescent cells is an important contributor to kidney aging, chronic renal disease, and poor outcome after kidney transplantation. Approaches to eliminate senescent cells with senolytic compounds have been proposed as novel strategies to improve marginal organs. While most existing senolytics induce senescent cell clearance by apoptosis, we observed that ferroptosis, an iron-catalyzed subtype of regulated necrosis, might serve as an alternative way to ablate senescent cells. We found that murine kidney tubular epithelial cells became sensitized to ferroptosis when turning senescent. This was linked to increased expression of pro-ferroptotic lipoxygenase-5 and reduced expression of anti-ferroptotic glutathione peroxidase 4 (GPX4). In tissue slice cultures from aged kidneys low dose application of the ferroptosis-inducer RSL3 selectively eliminated senescent cells while leaving healthy tubular cells unaffected. Similar results were seen in a transplantation model, in which RSL3 reduced the senescent cell burden of aged donor kidneys and caused a reduction of damage and inflammatory cell infiltration during the early post-transplantation period. In summary, these data reveal an increased susceptibility of senescent tubular cells to ferroptosis with the potential to be exploited for selective reduction of renal senescence in aged kidney transplants.
    MeSH term(s) Aging ; Animals ; Apoptosis ; Epithelial Cells ; Ferroptosis ; Mice
    Language English
    Publishing date 2022-06-08
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2060594-8
    ISSN 1600-6143 ; 1600-6135
    ISSN (online) 1600-6143
    ISSN 1600-6135
    DOI 10.1111/ajt.17102
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5542: Show issues Location:
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  5. Article: Cell Death Pathways Drive Necroinflammation during Acute Kidney Injury

    von Mässenhausen, Anne / Tonnus, Wulf / Linkermann, Andreas

    Nephron

    2018  Volume 140, Issue 2, Page(s) 144–147

    Abstract: Renal tubules represent an intercellular unit and function as a syncytium. When acute tubular necrosis was first visualized to occur through a process of synchronized regulated necrosis (SRN) in handpicked primary renal tubules, it became obvious that ... ...

    Institution Division of Nephrology, Department of Internal Medicine III, University Hospital Carl Gustav Carus at the Technische Universität Dresden, Dresden, Germany
    Abstract Renal tubules represent an intercellular unit and function as a syncytium. When acute tubular necrosis was first visualized to occur through a process of synchronized regulated necrosis (SRN) in handpicked primary renal tubules, it became obvious that SRN actually promotes nephron loss. This realization adds to our current understanding of acute kidney injury (AKI)-chronic kidney disease (CKD) transition and argues for the prevention of AKI episodes to prevent CKD progression. Because SRN is triggered by necroptosis and executed by ferroptosis, 2 recently identified signaling pathways of regulated necrosis, a combination therapy employing necrostatins and ferrostatins may be beneficial for protection against nephron loss. Clinical trials in AKI and during the process of kidney transplantation are now required to prevent SRN. Additionally, necrotic cell death drives autoimmunity and necroinflammation and therefore represents a therapeutic target even for the prevention of antibody-mediated rejection of allografts years after the transplantation process.
    Keywords Necroptosis ; Ferroptosis ; Pyroptosis ; Necroinflammation  ; Receptor-interacting protein kinase 3 ; Mixed lineage kinase domain-like ; Gasdermin ; Apoptosis ; Acute kidney injury-chronic kidney disease transition
    Language English
    Publishing date 2018-06-29
    Publisher S. Karger AG
    Publishing place Basel, Switzerland
    Document type Article
    Note Clinical Practice: Mini-Review
    ZDB-ID 207121-6
    ISSN 2235-3186 ; 1423-0186 ; 1660-8151 ; 0028-2766
    ISSN (online) 2235-3186 ; 1423-0186
    ISSN 1660-8151 ; 0028-2766
    DOI 10.1159/000490807
    Database Karger publisher's database

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  6. Article ; Online: Dipeptidase-1 governs renal inflammation during ischemia reperfusion injury.

    Lau, Arthur / Rahn, Jennifer J / Chappellaz, Mona / Chung, Hyunjae / Benediktsson, Hallgrimur / Bihan, Dominique / von Mässenhausen, Anne / Linkermann, Andreas / Jenne, Craig N / Robbins, Stephen M / Senger, Donna L / Lewis, Ian A / Chun, Justin / Muruve, Daniel A

    Science advances

    2022  Volume 8, Issue 5, Page(s) eabm0142

    Abstract: The mechanisms that drive leukocyte recruitment to the kidney are incompletely understood. Dipeptidase-1 (DPEP1) is a major neutrophil adhesion receptor highly expressed on proximal tubular cells and peritubular capillaries of the kidney. Renal ischemia ... ...

    Abstract The mechanisms that drive leukocyte recruitment to the kidney are incompletely understood. Dipeptidase-1 (DPEP1) is a major neutrophil adhesion receptor highly expressed on proximal tubular cells and peritubular capillaries of the kidney. Renal ischemia reperfusion injury (IRI) induces robust neutrophil and monocyte recruitment and causes acute kidney injury (AKI). Renal inflammation and the AKI phenotype were attenuated in
    MeSH term(s) Acute Kidney Injury/etiology ; Animals ; Dipeptidases/metabolism ; Female ; GPI-Linked Proteins/metabolism ; Humans ; Inflammation/complications ; Male ; Mice ; Mice, Inbred C57BL ; Reperfusion Injury
    Chemical Substances GPI-Linked Proteins ; Dipeptidases (EC 3.4.13.-) ; dipeptidase (EC 3.4.13.18) ; dipeptidase 1 (EC 3.4.13.19)
    Language English
    Publishing date 2022-02-02
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2810933-8
    ISSN 2375-2548 ; 2375-2548
    ISSN (online) 2375-2548
    ISSN 2375-2548
    DOI 10.1126/sciadv.abm0142
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  7. Article ; Online: Analysis of receptor tyrosine kinase gene amplification on the example of FGFR1.

    Boehm, Diana / von Mässenhausen, Anne / Perner, Sven

    Methods in molecular biology (Clifton, N.J.)

    2015  Volume 1233, Page(s) 67–79

    Abstract: FISH (fluorescent in situ hybridization) is a molecular cytogenetic method to detect large-scale genetic alterations in tissue and/or cells. Numerical aberrations (deletions and amplifications) and structural aberrations (translocations and fusions) are ... ...

    Abstract FISH (fluorescent in situ hybridization) is a molecular cytogenetic method to detect large-scale genetic alterations in tissue and/or cells. Numerical aberrations (deletions and amplifications) and structural aberrations (translocations and fusions) are detectable. Probes bind complementary to the DNA strand of the region of interest. Subsequently, the probes are detected via fluorochromes and appear as colored dots that can be assessed under the fluorescence microscope.In situ hybridization is divided into three steps: pretreatment, hybridization, and posthybridization. Pretreatment opens up the cell membranes for hybridization, so that the probe can bind to the complementary DNA target. Posthybridization includes washing steps to remove excessive probes and detection of probes via secondary marked fluorochromes. DAPI stains nuclei and serves as mounting media.
    MeSH term(s) Antibodies, Monoclonal/chemistry ; Antibodies, Monoclonal/metabolism ; Cells, Cultured ; Chromosome Aberrations ; Chromosomes, Artificial, Bacterial/chemistry ; Chromosomes, Artificial, Bacterial/metabolism ; DNA Probes/chemical synthesis ; DNA Probes/metabolism ; Fluorescent Antibody Technique ; Gene Amplification ; Gene Expression ; Humans ; In Situ Hybridization, Fluorescence/methods ; Lymphocytes/metabolism ; Lymphocytes/ultrastructure ; Metaphase ; Nucleic Acid Hybridization ; Permeability ; Receptor, Fibroblast Growth Factor, Type 1/genetics ; Receptor, Fibroblast Growth Factor, Type 1/metabolism ; Staining and Labeling/methods
    Chemical Substances Antibodies, Monoclonal ; DNA Probes ; FGFR1 protein, human (EC 2.7.10.1) ; Receptor, Fibroblast Growth Factor, Type 1 (EC 2.7.10.1)
    Language English
    Publishing date 2015
    Publishing country United States
    Document type Journal Article
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/978-1-4939-1789-1_7
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  8. Article ; Online: Immunological consequences of kidney cell death.

    Sarhan, Maysa / von Mässenhausen, Anne / Hugo, Christian / Oberbauer, Rainer / Linkermann, Andreas

    Cell death & disease

    2018  Volume 9, Issue 2, Page(s) 114

    Abstract: Death of renal cells is central to the pathophysiology of acute tubular necrosis, autoimmunity, necrotizing glomerulonephritis, cystic kidney disease, urosepsis, delayed graft function and transplant rejection. By means of regulated necrosis, immunogenic ...

    Abstract Death of renal cells is central to the pathophysiology of acute tubular necrosis, autoimmunity, necrotizing glomerulonephritis, cystic kidney disease, urosepsis, delayed graft function and transplant rejection. By means of regulated necrosis, immunogenic damage-associated molecular patterns (DAMPs) and highly reactive organelles such as lysosomes, peroxisomes and mitochondria are released from the dying cells, thereby causing an overwhelming immunologic response. The rupture of the plasma membrane exhibits the "point of no return" for the immunogenicity of regulated cell death, explaining why apoptosis, a highly organized cell death subroutine with long-lasting plasma membrane integrity, elicits hardly any immune response. Ferroptosis, an iron-dependent necrotic type cell death, results in the release of DAMPs and large amounts of lipid peroxides. In contrast, anti-inflammatory cytokines are actively released from cells that die by necroptosis, limiting the DAMP-induced immune response to a surrounding microenvironment, whereas at the same time, inflammasome-associated caspases drive maturation of intracellularly expressed interleukin-1β (IL-1β). In a distinct setting, additionally interleukin-18 (IL-18) is expressed during pyroptosis, initiated by gasdermin-mediated plasma membrane rupture. As all of these pathways are druggable, we provide an overview of regulated necrosis in kidney diseases with a focus on immunogenicity and potential therapeutic interventions.
    MeSH term(s) Animals ; Apoptosis ; Autoimmunity ; Humans ; Kidney/immunology ; Kidney/pathology ; Models, Biological ; Necrosis ; Signal Transduction
    Language English
    Publishing date 2018-01-25
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2541626-1
    ISSN 2041-4889 ; 2041-4889
    ISSN (online) 2041-4889
    ISSN 2041-4889
    DOI 10.1038/s41419-017-0057-9
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  9. Article ; Online: Gasdermin D-deficient mice are hypersensitive to acute kidney injury.

    Tonnus, Wulf / Maremonti, Francesca / Belavgeni, Alexia / Latk, Markus / Kusunoki, Yoshihiro / Brucker, Anne / von Mässenhausen, Anne / Meyer, Claudia / Locke, Sophie / Gembardt, Florian / Beer, Kristina / Hoppenz, Paul / Becker, Jan U / Hugo, Christian / Anders, Hans-Joachim / Bornstein, Stefan R / Shao, Feng / Linkermann, Andreas

    Cell death & disease

    2022  Volume 13, Issue 9, Page(s) 792

    Abstract: Signaling pathways of regulated necrosis, such as necroptosis and ferroptosis, contribute to acute kidney injury (AKI), but the role of pyroptosis is unclear. Pyroptosis is mediated by the pore-forming protein gasdermin D (GSDMD). Here, we report a ... ...

    Abstract Signaling pathways of regulated necrosis, such as necroptosis and ferroptosis, contribute to acute kidney injury (AKI), but the role of pyroptosis is unclear. Pyroptosis is mediated by the pore-forming protein gasdermin D (GSDMD). Here, we report a specific pattern of GSDMD-protein expression in the peritubular compartment of mice that underwent bilateral ischemia and reperfusion injury (IRI). Along similar lines, the GSDMD-protein expression in whole kidney lysates increased during the first 84 h following cisplatin-induced AKI. Importantly, unlike whole kidney lysates, no GSDMD-protein expression was detectable in isolated kidney tubules. In IRI and cisplatin-induced AKI, GSDMD-deficient mice exhibited hypersensitivity to injury as assessed by tubular damage, elevated markers of serum urea, and serum creatinine. This hypersensitivity was reversed by a combined deficiency of GSDMD and the necroptosis mediator mixed lineage kinase domain-like (MLKL). In conclusion, we demonstrate a non-cell autonomous role for GSDMD in protecting the tubular compartment from necroptosis-mediated damage in IRI.
    MeSH term(s) Acute Kidney Injury/metabolism ; Animals ; Cisplatin/adverse effects ; Creatinine ; Hypersensitivity ; Intracellular Signaling Peptides and Proteins/genetics ; Intracellular Signaling Peptides and Proteins/metabolism ; Mice ; Phosphate-Binding Proteins/genetics ; Phosphate-Binding Proteins/metabolism ; Urea
    Chemical Substances Intracellular Signaling Peptides and Proteins ; Phosphate-Binding Proteins ; Urea (8W8T17847W) ; Creatinine (AYI8EX34EU) ; Cisplatin (Q20Q21Q62J)
    Language English
    Publishing date 2022-09-15
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2541626-1
    ISSN 2041-4889 ; 2041-4889
    ISSN (online) 2041-4889
    ISSN 2041-4889
    DOI 10.1038/s41419-022-05230-9
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  10. Article ; Online: The pathological features of regulated necrosis.

    Tonnus, Wulf / Meyer, Claudia / Paliege, Alexander / Belavgeni, Alexia / von Mässenhausen, Anne / Bornstein, Stefan R / Hugo, Christian / Becker, Jan Ulrich / Linkermann, Andreas

    The Journal of pathology

    2019  Volume 247, Issue 5, Page(s) 697–707

    Abstract: Necrosis of a cell is defined by the loss of its plasma membrane integrity. Morphologically, necrosis occurs in several forms such as coagulative necrosis, colliquative necrosis, caseating necrosis, fibrinoid necrosis, and others. Biochemically, necrosis ...

    Abstract Necrosis of a cell is defined by the loss of its plasma membrane integrity. Morphologically, necrosis occurs in several forms such as coagulative necrosis, colliquative necrosis, caseating necrosis, fibrinoid necrosis, and others. Biochemically, necrosis was demonstrated to represent a number of genetically determined signalling pathways. These include (i) kinase-mediated necroptosis, which depends on receptor interacting protein kinase 3 (RIPK3)-mediated phosphorylation of the pseudokinase mixed lineage kinase domain like (MLKL); (ii) gasdermin-mediated necrosis downstream of inflammasomes, also referred to as pyroptosis; and (iii) an iron-catalysed mechanism of highly specific lipid peroxidation named ferroptosis. Given the molecular understanding of the nature of these pathways, specific antibodies may allow direct detection of regulated necrosis and correlation with morphological features. Necroptosis can be specifically detected by immunohistochemistry and immunofluorescence employing antibodies to phosphorylated MLKL. Likewise, it is possible to generate cleavage-specific antibodies against epitopes in gasdermin protein family members. In ferroptosis, however, specific detection requires quantification of oxidative lipids by mass spectrometry (oxylipidomics). Together with classical cell death markers, such as TUNEL staining and detection of cleaved caspase-3 in apoptotic cells, the extension of the arsenal of necrosis markers will allow pathological detection of specific molecular pathways rather than isolated morphological descriptions. These novel pieces of information will be extraordinarily helpful for clinicians as inhibitors of necroptosis (necrostatins), ferroptosis (ferrostatins), and inflammasomes have emerged in clinical trials. Anatomical pathologists should embrace these novel ancillary tests and the concepts behind them and test their impact on diagnostic precision, prognostication, and the prediction of response to the upcoming anti-necrotic therapies. Copyright © 2019 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
    MeSH term(s) Animals ; Apoptosis/physiology ; Cell Death/physiology ; Cell Membrane/pathology ; Disease Models, Animal ; Humans ; Inflammation/pathology ; Iron/metabolism ; Mice ; Necrosis/pathology
    Chemical Substances Iron (E1UOL152H7)
    Language English
    Publishing date 2019-02-25
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 3119-7
    ISSN 1096-9896 ; 0022-3417
    ISSN (online) 1096-9896
    ISSN 0022-3417
    DOI 10.1002/path.5248
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