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  1. Article ; Online: A guide to ferroptosis, the biological rust of cellular membranes.

    Veeckmans, Geraldine / Van San, Emily / Vanden Berghe, Tom

    The FEBS journal

    2023  

    Abstract: Unprotected iron can rust due to oxygen exposure. Similarly, in our body, oxidative stress can kill cells in an iron-dependent manner, which can give rise to devastating diseases. This type of cell death is referred to as ferroptosis. Generally, ... ...

    Abstract Unprotected iron can rust due to oxygen exposure. Similarly, in our body, oxidative stress can kill cells in an iron-dependent manner, which can give rise to devastating diseases. This type of cell death is referred to as ferroptosis. Generally, ferroptosis is defined as an iron-catalyzed form of regulated necrosis that occurs through excessive peroxidation of polyunsaturated fatty acids within cellular membranes. This review summarizes how ferroptosis is executed by a rather primitive biochemical process, under tight regulation of lipid, iron, and redox metabolic processes. An overview is given of major classes of ferroptosis inducers and inhibitors, and how to detect ferroptosis. Finally, its detrimental role in disease is briefly discussed.
    Language English
    Publishing date 2023-11-07
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2173655-8
    ISSN 1742-4658 ; 1742-464X
    ISSN (online) 1742-4658
    ISSN 1742-464X
    DOI 10.1111/febs.16993
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  2. Article ; Online: Viral dosing of influenza A infection reveals involvement of RIPK3 and FADD, but not MLKL.

    Oltean, Teodora / Van San, Emily / Divert, Tatyana / Vanden Berghe, Tom / Saelens, Xavier / Maelfait, Jonathan / Takahashi, Nozomi / Vandenabeele, Peter

    Cell death & disease

    2021  Volume 12, Issue 5, Page(s) 471

    Abstract: RIPK3 was reported to play an important role in the protection against influenza A virus (IAV) in vivo. Here we show that the requirement of RIPK3 for protection against IAV infection in vivo is only apparent within a limited dose range of IAV challenge. ...

    Abstract RIPK3 was reported to play an important role in the protection against influenza A virus (IAV) in vivo. Here we show that the requirement of RIPK3 for protection against IAV infection in vivo is only apparent within a limited dose range of IAV challenge. We found that this protective outcome is independent from RIPK3 kinase activity and from MLKL. This shows that platform function of RIPK3 rather than its kinase activity is required for protection, suggesting that a RIPK3 function independent of necroptosis is implicated. In line with this finding, we show that FADD-dependent apoptosis has a crucial additional effect in protection against IAV infection. Altogether, we show that RIPK3 contributes to protection against IAV in a narrow challenge dose range by a mechanism that is independent of its kinase activity and its capacity to induce necroptosis.
    MeSH term(s) Animals ; Fas-Associated Death Domain Protein/metabolism ; Humans ; Influenza A virus/genetics ; Mice ; Protein Kinases/metabolism ; Receptor-Interacting Protein Serine-Threonine Kinases/metabolism
    Chemical Substances Fadd protein, mouse ; Fas-Associated Death Domain Protein ; MLKL protein, mouse (EC 2.7.-) ; Protein Kinases (EC 2.7.-) ; Receptor-Interacting Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Ripk3 protein, mouse (EC 2.7.11.1)
    Language English
    Publishing date 2021-05-11
    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/s41419-021-03746-0
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Ferroptosis contributes to multiple sclerosis and its pharmacological targeting suppresses experimental disease progression.

    Van San, Emily / Debruyne, Angela C / Veeckmans, Geraldine / Tyurina, Yulia Y / Tyurin, Vladimir A / Zheng, Hao / Choi, Sze Men / Augustyns, Koen / van Loo, Geert / Michalke, Bernhard / Venkataramani, Vivek / Toyokuni, Shinya / Bayir, Hülya / Vandenabeele, Peter / Hassannia, Behrouz / Vanden Berghe, Tom

    Cell death and differentiation

    2023  Volume 30, Issue 9, Page(s) 2092–2103

    Abstract: Multiple sclerosis (MS) is a chronic autoimmune disorder characterized by central nervous (CNS) demyelination resulting in axonal injury and neurological deficits. Essentially, MS is driven by an auto-amplifying mechanism of inflammation and cell death. ... ...

    Abstract Multiple sclerosis (MS) is a chronic autoimmune disorder characterized by central nervous (CNS) demyelination resulting in axonal injury and neurological deficits. Essentially, MS is driven by an auto-amplifying mechanism of inflammation and cell death. Current therapies mainly focus on disease modification by immunosuppression, while no treatment specifically focuses on controlling cell death injury. Here, we report that ferroptosis, an iron-catalyzed mode of regulated cell death (RCD), contributes to MS disease progression. Active and chronic MS lesions and cerebrospinal fluid (CSF) of MS patients revealed several signs of ferroptosis, reflected by the presence of elevated levels of (labile) iron, peroxidized phospholipids and lipid degradation products. Treatment with our candidate lead ferroptosis inhibitor, UAMC-3203, strongly delays relapse and ameliorates disease progression in a preclinical model of relapsing-remitting MS. In conclusion, the results identify ferroptosis as a detrimental and targetable factor in MS. These findings create novel treatment options for MS patients, along with current immunosuppressive strategies.
    MeSH term(s) Humans ; Multiple Sclerosis/drug therapy ; Ferroptosis ; Multiple Sclerosis, Relapsing-Remitting/drug therapy ; Multiple Sclerosis, Relapsing-Remitting/cerebrospinal fluid ; Disease Progression ; Axons/metabolism ; Chronic Disease
    Language English
    Publishing date 2023-08-04
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 1225672-9
    ISSN 1476-5403 ; 1350-9047
    ISSN (online) 1476-5403
    ISSN 1350-9047
    DOI 10.1038/s41418-023-01195-0
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 4230: Show issues Location:
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    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)
    Zs.MG 80: Show issues

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  4. Article ; Online: Emerging immune and cell death mechanisms in stroke: Saponins as therapeutic candidates.

    García-Pupo, Laura / Van San, Emily / Delgado-Hernández, René / Vanden Berghe, Tom / Vanden Berghe, Wim

    Brain, behavior, & immunity - health

    2020  Volume 9, Page(s) 100152

    Abstract: The complexity of the ischemic cascade is based on the integrated crosstalk of every cell type in the neurovascular unit. Depending on the features of the ischemic insult, several cell death mechanisms are triggered, such as apoptosis, necroptosis, ... ...

    Abstract The complexity of the ischemic cascade is based on the integrated crosstalk of every cell type in the neurovascular unit. Depending on the features of the ischemic insult, several cell death mechanisms are triggered, such as apoptosis, necroptosis, ferroptosis/oxytosis, ETosis or pyroptosis, leading to reactive astrogliosis. However, emerging evidence demonstrates a dual role for the immune system in stroke pathophysiology, where it exerts both detrimental and also beneficial functions. In this review, we discuss the relevance of several cell death modalities and the dual role of the immune system in stroke pathophysiology. We also provide an overview of some emerging immunomodulatory therapeutic strategies, amongst which saponins, which are promising candidates that exert multiple pharmacological effects.
    Language English
    Publishing date 2020-10-03
    Publishing country United States
    Document type Journal Article ; Review
    ISSN 2666-3546
    ISSN (online) 2666-3546
    DOI 10.1016/j.bbih.2020.100152
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  5. Article ; Online: Fatal lymphocytic cardiac damage in coronavirus disease 2019 (COVID-19): autopsy reveals a ferroptosis signature.

    Jacobs, Werner / Lammens, Martin / Kerckhofs, Annelies / Voets, Evy / Van San, Emily / Van Coillie, Samya / Peleman, Cédric / Mergeay, Matthias / Sirimsi, Sabriya / Matheeussen, Veerle / Jansens, Hilde / Baar, Ingrid / Vanden Berghe, Tom / Jorens, Philippe G

    ESC heart failure

    2020  Volume 7, Issue 6, Page(s) 3772–3781

    Abstract: Aims: Cardiovascular complications, including myocarditis, are observed in coronavirus disease 2019 (COVID-19). Major cardiac involvement is a potentially lethal feature in severe cases. We sought to describe the underlying pathophysiological mechanism ... ...

    Abstract Aims: Cardiovascular complications, including myocarditis, are observed in coronavirus disease 2019 (COVID-19). Major cardiac involvement is a potentially lethal feature in severe cases. We sought to describe the underlying pathophysiological mechanism in COVID-19 lethal cardiogenic shock.
    Methods and results: We report on a 48-year-old male COVID-19 patient with cardiogenic shock; despite extracorporeal life support, dialysis, and massive pharmacological support, this rescue therapy was not successful. Severe acute respiratory syndrome coronavirus 2 RNA was detected at autopsy in the lungs and myocardium. Histopathological examination revealed diffuse alveolar damage, proliferation of type II pneumocytes, lymphocytes in the lung interstitium, and pulmonary microemboli. Moreover, patchy muscular, sometimes perivascular, interstitial mononuclear inflammatory infiltrates, dominated by lymphocytes, were seen in the cardiac tissue. The lymphocytes 'interlocked' the myocytes, resulting in myocyte degeneration and necrosis. Predominantly, T-cell lymphocytes with a CD4:CD8 ratio of 1.7 infiltrated the interstitial myocardium, reflecting true myocarditis. The myocardial tissue was examined for markers of ferroptosis, an iron-catalysed form of regulated cell death that occurs through excessive peroxidation of polyunsaturated fatty acids. Immunohistochemical staining with E06, a monoclonal antibody binding to oxidized phosphatidylcholine (reflecting lipid peroxidation during ferroptosis), was positive in morphologically degenerating and necrotic cardiomyocytes adjacent to the infiltrate of lymphocytes, near arteries, in the epicardium and myocardium. A similar ferroptosis signature was present in the myocardium of a COVID-19 subject without myocarditis. In a case of sudden death due to viral myocarditis of unknown aetiology, however, immunohistochemical staining with E06 was negative. The renal proximal tubuli stained positively for E06 and also hydroxynonenal (4-HNE), a reactive breakdown product of the lipid peroxides that execute ferroptosis. In the case of myocarditis of other aetiology, the renal tissue displayed no positivity for E06 or 4-HNE.
    Conclusions: The findings in this case are unique as this is the first report on accumulated oxidized phospholipids (or their breakdown products) in myocardial and renal tissue in COVID-19. This highlights ferroptosis, proposed to detrimentally contribute to some forms of ischaemia-reperfusion injury, as a detrimental factor in COVID-19 cardiac damage and multiple organ failure.
    Keywords covid19
    Language English
    Publishing date 2020-09-22
    Publishing country England
    Document type Journal Article
    ZDB-ID 2814355-3
    ISSN 2055-5822 ; 2055-5822
    ISSN (online) 2055-5822
    ISSN 2055-5822
    DOI 10.1002/ehf2.12958
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  6. Article: Fatal lymphocytic cardiac damage in coronavirus disease 2019 (COVID-19): autopsy reveals a ferroptosis signature

    Jacobs, Werner / Lammens, Martin / Kerckhofs, Annelies / Voets, Evy / Van San, Emily / Van Coillie, Samya / Peleman, Cédric / Mergeay, Matthias / Sirimsi, Sabriya / Matheeussen, Veerle / Jansens, Hilde / Baar, Ingrid / Vanden Berghe, Tom / Jorens, Philippe G

    ESC Heart Fail

    Abstract: AIMS: Cardiovascular complications, including myocarditis, are observed in coronavirus disease 2019 (COVID-19). Major cardiac involvement is a potentially lethal feature in severe cases. We sought to describe the underlying pathophysiological mechanism ... ...

    Abstract AIMS: Cardiovascular complications, including myocarditis, are observed in coronavirus disease 2019 (COVID-19). Major cardiac involvement is a potentially lethal feature in severe cases. We sought to describe the underlying pathophysiological mechanism in COVID-19 lethal cardiogenic shock. METHODS AND RESULTS: We report on a 48-year-old male COVID-19 patient with cardiogenic shock; despite extracorporeal life support, dialysis, and massive pharmacological support, this rescue therapy was not successful. Severe acute respiratory syndrome coronavirus 2 RNA was detected at autopsy in the lungs and myocardium. Histopathological examination revealed diffuse alveolar damage, proliferation of type II pneumocytes, lymphocytes in the lung interstitium, and pulmonary microemboli. Moreover, patchy muscular, sometimes perivascular, interstitial mononuclear inflammatory infiltrates, dominated by lymphocytes, were seen in the cardiac tissue. The lymphocytes 'interlocked' the myocytes, resulting in myocyte degeneration and necrosis. Predominantly, T-cell lymphocytes with a CD4:CD8 ratio of 1.7 infiltrated the interstitial myocardium, reflecting true myocarditis. The myocardial tissue was examined for markers of ferroptosis, an iron-catalysed form of regulated cell death that occurs through excessive peroxidation of polyunsaturated fatty acids. Immunohistochemical staining with E06, a monoclonal antibody binding to oxidized phosphatidylcholine (reflecting lipid peroxidation during ferroptosis), was positive in morphologically degenerating and necrotic cardiomyocytes adjacent to the infiltrate of lymphocytes, near arteries, in the epicardium and myocardium. A similar ferroptosis signature was present in the myocardium of a COVID-19 subject without myocarditis. In a case of sudden death due to viral myocarditis of unknown aetiology, however, immunohistochemical staining with E06 was negative. The renal proximal tubuli stained positively for E06 and also hydroxynonenal (4-HNE), a reactive breakdown product of the lipid peroxides that execute ferroptosis. In the case of myocarditis of other aetiology, the renal tissue displayed no positivity for E06 or 4-HNE. CONCLUSIONS: The findings in this case are unique as this is the first report on accumulated oxidized phospholipids (or their breakdown products) in myocardial and renal tissue in COVID-19. This highlights ferroptosis, proposed to detrimentally contribute to some forms of ischaemia-reperfusion injury, as a detrimental factor in COVID-19 cardiac damage and multiple organ failure.
    Keywords covid19
    Publisher WHO
    Document type Article
    Note WHO #Covidence: #777436
    Database COVID19

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  7. Article ; Online: Fatal lymphocytic cardiac damage in coronavirus disease 2019 (COVID‐19)

    Jacobs, Werner / Lammens, Martin / Kerckhofs, Annelies / Voets, Evy / Van San, Emily / Van Coillie, Samya / Peleman, Cédric / Mergeay, Matthias / Sirimsi, Sabriya / Matheeussen, Veerle / Jansens, Hilde / Baar, Ingrid / Vanden Berghe, Tom / Jorens, Philippe G.

    ESC Heart Failure ; ISSN 2055-5822 2055-5822

    autopsy reveals a ferroptosis signature

    2020  

    Keywords covid19
    Language English
    Publisher Wiley
    Publishing country us
    Document type Article ; Online
    DOI 10.1002/ehf2.12958
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  8. Article ; Online: Targeting ferroptosis protects against experimental (multi)organ dysfunction and death.

    Van Coillie, Samya / Van San, Emily / Goetschalckx, Ines / Wiernicki, Bartosz / Mukhopadhyay, Banibrata / Tonnus, Wulf / Choi, Sze Men / Roelandt, Ria / Dumitrascu, Catalina / Lamberts, Ludwig / Dams, Geert / Weyts, Wannes / Huysentruyt, Jelle / Hassannia, Behrouz / Ingold, Irina / Lele, Suhas / Meyer, Evelyne / Berg, Maya / Seurinck, Ruth /
    Saeys, Yvan / Vermeulen, An / van Nuijs, Alexander L N / Conrad, Marcus / Linkermann, Andreas / Rajapurkar, Mohan / Vandenabeele, Peter / Hoste, Eric / Augustyns, Koen / Vanden Berghe, Tom

    Nature communications

    2022  Volume 13, Issue 1, Page(s) 1046

    Abstract: The most common cause of death in the intensive care unit (ICU) is the development of multiorgan dysfunction syndrome (MODS). Besides life-supporting treatments, no cure exists, and its mechanisms are still poorly understood. Catalytic iron is associated ...

    Abstract The most common cause of death in the intensive care unit (ICU) is the development of multiorgan dysfunction syndrome (MODS). Besides life-supporting treatments, no cure exists, and its mechanisms are still poorly understood. Catalytic iron is associated with ICU mortality and is known to cause free radical-mediated cellular toxicity. It is thought to induce excessive lipid peroxidation, the main characteristic of an iron-dependent type of cell death conceptualized as ferroptosis. Here we show that the severity of multiorgan dysfunction and the probability of death are indeed associated with plasma catalytic iron and lipid peroxidation. Transgenic approaches underscore the role of ferroptosis in iron-induced multiorgan dysfunction. Blocking lipid peroxidation with our highly soluble ferrostatin-analogue protects mice from injury and death in experimental non-septic multiorgan dysfunction, but not in sepsis-induced multiorgan dysfunction. The limitations of the experimental mice models to mimic the complexity of clinical MODS warrant further preclinical testing. In conclusion, our data suggest ferroptosis targeting as possible treatment option for a stratifiable subset of MODS patients.
    MeSH term(s) Animals ; Cell Death ; Ferroptosis ; Humans ; Iron/metabolism ; Lipid Peroxidation ; Mice ; Multiple Organ Failure/prevention & control
    Chemical Substances Iron (E1UOL152H7)
    Language English
    Publishing date 2022-02-24
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-022-28718-6
    Database MEDical Literature Analysis and Retrieval System OnLINE

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