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Article ; Online: Cholesterol business: life or death by rust.

Gavali, Shubhangi / Maremonti, Francesca / Linkermann, Andreas

Signal transduction and targeted therapy

2024 Volume 9, Issue 1, Page(s) 71

Language	English
Publishing date	2024-03-21
Publishing country	England
Document type	Journal Article
ZDB-ID	2886872-9
ISSN	2059-3635 ; 2095-9907
ISSN (online)	2059-3635
ISSN	2095-9907
DOI	10.1038/s41392-024-01802-7
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Article ; Online: Protocol for isolating murine kidney tubules and ex vivo cell death assays.

Belavgeni, Alexia / Maremonti, Francesca / Linkermann, Andreas

STAR protocols

2024 Volume 5, Issue 2, Page(s) 103005

Abstract: Isolating kidney tubules offers insights into their biological function without stroma, vascular cells, and immune system interference. Our murine tubule isolation protocol focuses on ex vivo cell death assays. We describe steps for solution preparation; ...

Abstract	Isolating kidney tubules offers insights into their biological function without stroma, vascular cells, and immune system interference. Our murine tubule isolation protocol focuses on ex vivo cell death assays. We describe steps for solution preparation; kidney extraction, decapsulation, and slicing; and tubule isolation. We also outline assays like western blotting, lactate dehydrogenase release assay, and live-cell imaging of vital dyes during experimental acute tubular necrosis. This adaptable protocol allows the generation of outgrown primary tubular cells that maintain the features of tubular cells.
Language	English
Publishing date	2024-04-11
Publishing country	United States
Document type	Journal Article
ISSN	2666-1667
ISSN (online)	2666-1667
DOI	10.1016/j.xpro.2024.103005
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Article ; Online: Mechanisms and Models of Kidney Tubular Necrosis and Nephron Loss.

Maremonti, Francesca / Meyer, Claudia / Linkermann, Andreas

Journal of the American Society of Nephrology : JASN

2022 Volume 33, Issue 3, Page(s) 472–486

Abstract: Understanding nephron loss is a primary strategy for preventing CKD progression. Death of renal tubular cells may occur by apoptosis during developmental and regenerative processes. However, during AKI, the transition of AKI to CKD, sepsis-associated AKI, ...

Abstract	Understanding nephron loss is a primary strategy for preventing CKD progression. Death of renal tubular cells may occur by apoptosis during developmental and regenerative processes. However, during AKI, the transition of AKI to CKD, sepsis-associated AKI, and kidney transplantation ferroptosis and necroptosis, two pathways associated with the loss of plasma membrane integrity, kill renal cells. This necrotic type of cell death is associated with an inflammatory response, which is referred to as necroinflammation. Importantly, the necroinflammatory response to cells that die by necroptosis may be fundamentally different from the tissue response to ferroptosis. Although mechanisms of ferroptosis and necroptosis have recently been investigated in detail, the cell death propagation during tubular necrosis, although described morphologically, remains incompletely understood. Here, we argue that a molecular switch downstream of tubular necrosis determines nephron regeneration versus nephron loss. Unraveling the details of this "switch" must include the inflammatory response to tubular necrosis and regenerative signals potentially controlled by inflammatory cells, including the stimulation of myofibroblasts as the origin of fibrosis. Understanding in detail the molecular switch and the inflammatory responses to tubular necrosis can inform the discussion of therapeutic options.
MeSH term(s)	Acute Kidney Injury/metabolism ; Apoptosis ; Female ; Humans ; Kidney/metabolism ; Kidney Cortex Necrosis ; Male ; Necrosis/drug therapy ; Nephrons/metabolism ; Renal Insufficiency, Chronic/metabolism
Language	English
Publishing date	2022-01-12
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	1085942-1
ISSN	1533-3450 ; 1046-6673
ISSN (online)	1533-3450
ISSN	1046-6673
DOI	10.1681/ASN.2021101293
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Article ; Online: Schwann cell necroptosis in diabetic neuropathy.

Belavgeni, Alexia / Maremonti, Francesca / Stadtmüller, Marlena / Bornstein, Stefan R / Linkermann, Andreas

Proceedings of the National Academy of Sciences of the United States of America

2022 Volume 119, Issue 17, Page(s) e2204049119

MeSH term(s)	Diabetes Mellitus ; Diabetic Neuropathies ; Humans ; Necroptosis ; Schwann Cells ; Sciatic Nerve
Language	English
Publishing date	2022-04-21
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2204049119
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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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Article ; Online: Treatment with siRNAs is commonly associated with GPX4 up-regulation and target knockdown-independent sensitization to ferroptosis.

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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Article ; Online: COVID-19 and Diabetic Nephropathy.

Maremonti, Francesca / Locke, Sophie / Tonnus, Wulf / Beer, Kristina / Brucker, Anne / Gonzalez, Nadia Zamora / Latk, Marcus / Belavgeni, Alexia / Hoppenz, Paul / Hugo, Christian / Linkermann, Andreas

Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme

2022 Volume 54, Issue 8, Page(s) 510–513

Abstract: Diabetic nephropathy is the most common condition that requires a chronic renal replacement therapy, such as hemodialysis, peritoneal dialysis, kidney transplantation, or simultaneous kidney-pancreas transplantation. Chronic kidney disease progression, ... ...

Abstract	Diabetic nephropathy is the most common condition that requires a chronic renal replacement therapy, such as hemodialysis, peritoneal dialysis, kidney transplantation, or simultaneous kidney-pancreas transplantation. Chronic kidney disease progression, that is the loss of nephrons, which causes the continuous decline of the eGFR, underlies the pathogenesis of diabetic nephropathy. During the COVID-19 pandemic, it became clear that diabetic nephropathy is amongst the independent risk factors that predicts unfavourable outcome upon SARS-CoV2 infection. While we still lack conclusive mechanistic insights into how nephrons are rapidly lost upon SARS-CoV2 infection and why patients with diabetic nephropathy are more susceptible to severe outcomes upon SARS-CoV2 infection, here, we discuss several aspects of the interface of COVID-19 with diabetic nephropathy. We identify the shortage of reliable rodent models of diabetic nephropathy, limited treatment options for human diabetic nephropathy and the lack of knowledge about virus-induced signalling pathways of regulated necrosis, such as necroptosis, as key factors that explain our failure to understand this system. Finally, we focus on immunosuppressed patients and discuss vaccination efficacy in these and diabetic patients. We conclude that more basic science and mechanistic understanding will be required both in diabetic nephropathy as well as in host immune responses to the SARS-CoV2 virus if novel therapeutic strategies are desired.
MeSH term(s)	COVID-19 ; Diabetes Mellitus ; Diabetic Nephropathies/pathology ; Humans ; Kidney Failure, Chronic ; Pandemics ; RNA, Viral ; SARS-CoV-2
Chemical Substances	RNA, Viral
Language	English
Publishing date	2022-04-06
Publishing country	Germany
Document type	Journal Article
ZDB-ID	80125-2
ISSN	1439-4286 ; 0018-5043
ISSN (online)	1439-4286
ISSN	0018-5043
DOI	10.1055/a-1819-4822
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Zs.A 681: Show issues

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ab Jg. 2022: Lesesaal (EG)

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Article ; Online: Dexamethasone sensitizes to ferroptosis by glucocorticoid receptor-induced dipeptidase-1 expression and glutathione depletion.

von Mässenhausen, Anne / Zamora Gonzalez, Nadia / Maremonti, Francesca / Belavgeni, Alexia / Tonnus, Wulf / Meyer, Claudia / Beer, Kristina / Hannani, Monica T / Lau, Arthur / Peitzsch, Mirko / Hoppenz, Paul / Locke, Sophie / Chavakis, Triantafyllos / Kramann, Rafael / Muruve, Daniel A / Hugo, Christian / Bornstein, Stefan R / Linkermann, Andreas

Science advances

2022 Volume 8, Issue 5, Page(s) eabl8920

Abstract: Dexamethasone is widely used as an immunosuppressive therapy and recently as COVID-19 treatment. Here, we demonstrate that dexamethasone sensitizes to ferroptosis, a form of iron-catalyzed necrosis, previously suggested to contribute to diseases such as ... ...

Abstract	Dexamethasone is widely used as an immunosuppressive therapy and recently as COVID-19 treatment. Here, we demonstrate that dexamethasone sensitizes to ferroptosis, a form of iron-catalyzed necrosis, previously suggested to contribute to diseases such as acute kidney injury, myocardial infarction, and stroke, all of which are triggered by glutathione (GSH) depletion. GSH levels were significantly decreased by dexamethasone. Mechanistically, we identified that dexamethasone up-regulated the GSH metabolism regulating protein dipeptidase-1 (DPEP1) in a glucocorticoid receptor (GR)-dependent manner. DPEP1 knockdown reversed the phenotype of dexamethasone-induced ferroptosis sensitization. Ferroptosis inhibitors, the DPEP1 inhibitor cilastatin, or genetic
MeSH term(s)	Carbolines/adverse effects ; Carbolines/pharmacology ; Cell Line ; Dexamethasone/pharmacology ; Dipeptidases/genetics ; Dipeptidases/metabolism ; Ferroptosis/drug effects ; Ferroptosis/genetics ; Fluorescent Antibody Technique ; GPI-Linked Proteins/genetics ; GPI-Linked Proteins/metabolism ; Gene Expression Regulation/drug effects ; Gene Knockdown Techniques ; Glutathione/metabolism ; Humans ; Immunophenotyping ; Oxidation-Reduction/drug effects ; Piperazines/adverse effects ; Piperazines/pharmacology ; Receptors, Glucocorticoid/metabolism
Chemical Substances	Carbolines ; GPI-Linked Proteins ; Piperazines ; RSL3 compound ; Receptors, Glucocorticoid ; erastin ; Dexamethasone (7S5I7G3JQL) ; Dipeptidases (EC 3.4.13.-) ; dipeptidase 1 (EC 3.4.13.19) ; Glutathione (GAN16C9B8O)
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.abl8920
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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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Article ; Online: vPIF-1 is an insulin-like antiferroptotic viral peptide.

Proceedings of the National Academy of Sciences of the United States of America

2023 Volume 120, Issue 21, Page(s) e2300320120

Abstract: Iridoviridae, such as the lymphocystis disease virus-1 (LCDV-1) and other viruses, encode viral insulin-like peptides (VILPs) which are capable of triggering insulin receptors (IRs) and insulin-like growth factor receptors. The homology of VILPs includes ...

Abstract	Iridoviridae, such as the lymphocystis disease virus-1 (LCDV-1) and other viruses, encode viral insulin-like peptides (VILPs) which are capable of triggering insulin receptors (IRs) and insulin-like growth factor receptors. The homology of VILPs includes highly conserved disulfide bridges. However, the binding affinities to IRs were reported to be 200- to 500-fold less effective compared to the endogenous ligands. We therefore speculated that these peptides also have noninsulin functions. Here, we report that the LCDV-1 VILP can function as a potent and highly specific inhibitor of ferroptosis. Induction of cell death by the ferroptosis inducers erastin, RSL3, FIN56, and FINO2 and nonferroptotic necrosis produced by the thioredoxin-reductase inhibitor ferroptocide were potently prevented by LCDV-1, while human insulin had no effect. Fas-induced apoptosis, necroptosis, mitotane-induced cell death and growth hormone-releasing hormone antagonist-induced necrosis were unaffected, suggesting the specificity to ferroptosis inhibition by the LCDV-1 VILP. Mechanistically, we identified the viral C-peptide to be required for inhibition of lipid peroxidation and ferroptosis inhibition, while the human C-peptide exhibited no antiferroptotic properties. In addition, the deletion of the viral C-peptide abolishes radical trapping activity in cell-free systems. We conclude that iridoviridae, through the expression of insulin-like viral peptides, are capable of preventing ferroptosis. In analogy to the viral mitochondrial inhibitor of apoptosis and the viral inhibitor of RIP activation (vIRA) that prevents necroptosis, we rename the LCDV-1 VILP a viral peptide inhibitor of ferroptosis-1. Finally, our findings indicate that ferroptosis may function as a viral defense mechanism in lower organisms.
MeSH term(s)	Humans ; Insulin ; C-Peptide ; Apoptosis ; Necrosis ; Cell Death
Chemical Substances	Insulin ; C-Peptide
Language	English
Publishing date	2023-05-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2300320120
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