Is this you? As a journalist, you can create a free Muck Rack account to customize your profile, list your contact preferences, and upload a portfolio of your best work.
Claim your profile
Articles by Marcus Conrad
Mechanisms of regeneration and maladaptive repair in acute kidney injury
Abstract Acute kidney injury (AKI) is a major risk factor for the subsequent development and progression of chronic kidney disease (CKD), particularly when kidney repair is incomplete or maladaptive. The repair trajectory after kidney injury is primarily determined through the interconnected responses of tubular epithelial cells (TECs), immune cells and fibroblasts. Within this network, TECs act as sentinels of tissue injury and initiators of the repair cascade.
Resolving the subcellular redox landscape of Coenzyme Q
Keywords CoQ subcellular fractionation dual-isotope-based oxidation correction mass spectrometry ferroptosis redox biochemistry clinical biomarker Introduction Coenzyme Q10 (CoQ10) and its reduced form, CoQ10H2, are essential regulators of cellular homeostasis. In mitochondria, CoQ10 functions as an electron carrier in the electron transport chain (ETC), shuttling electrons from complexes I, II, and CoQ-linked enzymes such as dihydroorotate dehydrogenase (DHODH) to complex III.
Molecular Targets and Therapeutics Center
Unser Ziel ist die Entschlüsselung von biologischen Signalwegen und molekularen Mechanismen, die physiologische und krankheitsbezogene zelluläre Prozesse steuern, und damit neue Zielstrukturen zu identifizieren und innovative therapeutische Konzepte zu entwickeln. Auf dieser Seite Forschungsbereiche Highlights Institutsleiter Institute Plattformen Forschungsgruppen Publikationen Kontakt Zelltod und Immunität Fehlgeleitete Signalprozesse sind Auslöser vieler Krankheiten.
Author Correction: 7-Dehydrocholesterol is an endogenous suppressor of ferroptosis
|
Correction to: Nature https://doi.org/10.1038/s41586-023-06878-9 Published online 31 January 2024 In the originally published version of this article, the blank values in Extended Data Fig. 2a,b correspond to background fluorescence measurements of a stable commercial resazurin solution (AquaBluer Cell Viability Assay Solution, Multi-Target Pharmaceuticals, cat. no. 6015), diluted in complete culture medium.
By Florencio Porto Freitas, Hamed Alborzinia, Palina Nepachalovich, Lohans Pedrera, Omkar Zilka, Alex Inague, Corinna Klein, Nesrine Aroua, Kamini Kaushal, Bettina Kast, Svenja Lorenz Verified, Zhiyi Chen, Sena Atici, Sebastian Doll, Emily Schaefer, Werner Schmitz, Peter Imming, Sayuri Miyamoto, Ann M. Wehman, Karoly Mirnics, Lokender Kumar, Judith Klein-Seetharaman, Svenja Meierjohann, Isabel Weigand, Matthias Kroiss, Georg W. Bornkamm, Fernando Gomes, Manjima B Sathian, David B. Konrad, Douglas Covey, Bernhard Michalke, Kurt Bommert, Ralf Bargou, Ana J. García-Sáez, Derek Pratt, Maria Fedorova, Andreas Trumpp, Marcus Conrad, Viktoria Kunz, Helene Nehring, Ifedapo Ekpo, Aline Horling, Thiago C. Genaro-Mattos
|
Nature
Verified
Riboflavin metabolism shapes FSP1-driven ferroptosis resistance
|
Abstract Membrane protection against oxidative insults is achieved by the concerted action of glutathione peroxidase 4 (GPX4) and endogenous lipophilic antioxidants such as ubiquinone and vitamin E. More recently, ferroptosis suppressor protein 1 (FSP1) was identified as a critical ferroptosis inhibitor, acting via the regeneration of membrane-embedded antioxidants.
By Izadora de Souza, Biplab Ghosh, Florencio Porto Freitas, Zhiyi Chen, Shibo Sun, Palina Nepachalovich, Juliane Tschuck, Apoorva Mathur, Ariane Nunes-Alves, Jannik Buhr, Camilo Aponte-Santamaría, Werner Schmitz, Matthias Mack, Martin Eilers, Ralf Bargou, Milena Chaufan, Mayher Kaur, Mario Palma, Jessalyn M. Ubellacker, Ulrich Elling, Hellmut G. Augustin, Kamyar Hadian, Svenja Meierjohann, Bettina Proneth, Marcus Conrad, Maria Fedorova, Hamed Alborzinia, Vera Skafar, Merce Donate Castillo, Lars Seufert, Sebastian Bothe
|
Nature
Verified
Fat bolsters tumours against ferroptosis
Tumour location dictates ferroptosis resistance. A study indicates that peritumoural adipose tissue aids tumours in evading ferroptosis by supplying tryptophan metabolites, including kynurenine and 3-hydroxykynurenine, which block NCOA4-mediated ferritinophagy to lower levels of labile iron and suppress lipid peroxidation.
A fin-loop-like structure in GPX4 underlies neuroprotection from ferroptosis
|
Keywords ferroptosis GPX4 Alzheimer’s disease neurodegeneration cell death neuroinflammation spondylometaphyseal dysplasia Sedaghatian type SSMD Introduction The progressive loss of neurons is a recurring feature of neurodegenerative diseases, a diverse group of disorders characterized by cognitive decline, motor impairment, and, in many cases, premature death.1,2,3,4 Although neuronal death is a shared endpoint, each neurodegenerative condition presents with distinct pathological hallmarks,...
By Svenja Lorenz Verified, Adam Wahida, Mark J. Bostock, Tobias Seibt, Anastasia Levkina, Dietrich Trümbach, Mohamed Soudy, David Emler, Nicola Rothammer, Marcel S. Woo, Jana K. Sonner, Mariia Novikova, Bernhard Henkelmann, Maceler Aldrovandi, Daniel F. Kaemena, Eikan Mishima, Perrine Vermonden, Zhi Zong, Deng Cheng, Toshitaka Nakamura, Junya Ito, Sebastian Doll, Bettina Proneth, Erika Bürkle, Francesca Rizzollo, Abril Escamilla Ayala, Valeria Napolitano, Marta Kolonko-Adamska, Stefan Gaussmann, Juliane Merl-Pham, Stefanie Hauck, Anna Pertek, Tanja Orschmann, Emily Van San, Tom Vanden Berghe, Daniela Hass, Adriano Maida, Joris M. Frenz, Lohans Pedrera, Amalia M. Dolga, Markus Kraiger, Helmut Fuchs, Gregor Ebert, Jerica Lenberg, Jennifer Friedman, Patrizia Agostinis, Annemarie Zimprich, Daniela Vogt-Weisenhorn, Lillian Garrett, Sabine M. Hölter, Wolfgang Wurst, Enrico Glaab, Jan Lewerenz, Bastian Popper, Christian Sieben Verified, Petra Steinacker, Hans Zischka, Ana J. García-Sáez, Anna Tietze, Sanath Kumar Ramesh, Scott Ayton, Michelle Vincendeau, Manuel A. Friese, Kristen Wigby, Michael Sattler, Matthias Mann, Irina Ingold, Ashok Kumar Jayavelu, Grzegorz M. Popowicz, Marcus Conrad
|
Cell Press
Verified
Lymph node environment drives FSP1 targetability in metastasizing melanoma
|
Abstract Ferroptosis has emerged as an actionable target to eliminate therapy-resistant and metastatic cancers1. However, which ferroptosis surveillance systems may offer a therapeutic window to leverage redox maladaptation in cancer remains unclear. In melanoma, glutathione peroxidase 4 (GPX4) impedes ferroptosis during haematogenous metastasis, but is dispensable during lymphatic metastasis2.
By Mario Palma, Milena Chaufan, Cort B. Breuer, Sebastian Müller, Marie Sabatier, Cameron Fraser, Krystina J. Szylo, Mahsa Yavari, Alanis Carmona, Mayher Kaur, Feyza Cansiz, June Monge-Lorenzo, Midori Flores, Eikan Mishima, Toshitaka Nakamura, Bettina Proneth, Marcos Labrado, Yanshan Liang, Nicole Cayting, Lan Zheng, Tatiana Cañeque, Ludovic Colombeau, Adam Wahida, Alpaslan Tasdogan, Sheng Hui, Raphaël Rodriguez, Marcus Conrad, Nathan E. Reticker-Flynn, Jessalyn M. Ubellacker
|
Nature
Verified
Targeting FSP1 triggers ferroptosis in lung cancer
|
Abstract Emerging evidence indicates that cancer cells are susceptible to ferroptosis, a form of cell death that is triggered by uncontrolled lipid peroxidation1,2,3. Despite broad enthusiasm about harnessing ferroptosis as a novel anti-cancer strategy, whether ferroptosis is a barrier to tumorigenesis and can be leveraged therapeutically remains unknown4,5.
By Katherine C. Wu, Alec J Vaughan, Jozef P. Bossowski, Yuan Hao, Aikaterini Ziogou, Seon Min Kim, Mari N Nakamura, Ray Pillai, Mariana Mancini, Sahith Rajalingam, Mingqi Han, Toshitaka Nakamura, Lidong Wang, Suckwoo Chung, Diane Simeone, David Shackelford, Yun Pyo Kang, Marcus Conrad, Thales Papagiannakopoulos
|
Nature
Verified
Decoding ferroptosis for cancer therapy - Nature Reviews Cancer
Abstract Resisting cell death is a pivotal hallmark of cancer and one of several increasingly actionable functional capabilities acquired by cancer cells to sustain their malignant state. Since the early 2000s, the discovery of multiple regulated cell death programmes has intensified interest in targeting these maladaptive traits that cancer cells employ to resist cellular demise.
Author Correction: Targeting ferroptosis protects against experimental (multi)organ dysfunction and death - Nature Communications
Correction to: Nature Communications https://doi.org/10.1038/s41467-022-28718-6, published online 24 February 2022 In the version of the article initially published, due to a calibration error, values for malondialdehyde (MDA) concentrations reported in the Results, Methods, Fig. 1 and Supp Figs. 1, 2 were underestimated by a factor of five.
Six ERC Grants for TUM researchers
Prof. Dr. Pramod Bhatotia Cloud computing platforms are based on distributed systems, in which several computers work together independently. However, distributed systems are vulnerable to attacks and failures, particularly in large, complex environments. Current solutions often have limitations, particularly with regard to programmability, security, and performance.
Skip to main contentSkip to main content You have permission to edit this image. You don't have any notifications. Get up-to-the-minute news sent straight to your device. Topics Breaking News Subscribe News Alert Subscribe Secure transaction. Cancel anytime. Have an account? Log In Account processing issue - the email address may already exist User information Username (Optional) This is the name that will be used to identify you within the system.
N-acetyl-l-cysteine averts ferroptosis by fostering glutathione peroxidase 4
Keywords ferroptosis NAC d-NAC cysteine system xc− xCT GSH GPX4 FSP1 β-ME Introduction N-acetyl-l-cysteine (NAC), an acetylated derivative of the amino acid l-cysteine, is used in the treatment of various pathological conditions, including autoimmune diseases, metabolic disorders, and neurological and psychiatric disorders, while its mechanism of action remains incompletely understood.1 Traditionally, the biological effects of NAC were attributed to its roles in disulfide reduction and...
Interplay of ferroptotic and apoptotic cell death and its modulation by BH3-mimetics - Cell Death & Differentiation
Abstract Ferroptosis and apoptosis are widely considered to be independent cell death modalities. Ferroptotic cell death is a consequence of insufficient radical detoxification and progressive lipid peroxidation, which is counteracted by glutathione peroxidase-4 (GPX4). Apoptotic cell death can be triggered by a wide variety of stresses, including oxygen radicals, and can be suppressed by anti-apoptotic members of the BCL-2 protein family.
Ferroptosis: when metabolism meets cell death
*Correspondence:marcus.conrad@helmholtz-munich.de Institute of Metabolism and Cell Death, Molecular Targets and Therapeutics Center, Helmholtz Zentrum München, Ingolstädter Landstr. 1, 85764 Neuherberg, Germany Translational Redox Biology, Technical University of Munich (TUM), TUM Natural School of Sciences, 85748 Garching, Germany
PRDX6 dictates ferroptosis sensitivity by directing cellular selenium utilization
|
Keywords GPX4 lipid peroxidation cell death cysteine selenocysteine selenoproteins selenite LC-MS/MS tumor brain Introduction Ferroptosis, a regulated cell death modality hallmarked by unrestrained iron-dependent (phospho)lipid peroxidation,1 has emerged as an important facet of redox cell biology and a promising target for treating human disease.2,3,4 Notably, its potential efficacy against (chemo)therapy-resistant and metastasizing cancers positions ferroptosis as a highly promising target...
By Junya Ito, Toshitaka Nakamura, Takashi Toyama, Deng Chen, Carsten Berndt, Gereon Poschmann, Sebastian Doll, Mirai Suzuki, Weijia Zhang, Jiashuo Zheng, Dietrich Trümbach, Naoya Yamada, Masana Yazaki, Mieko Arisawa, Yusuke Ohsaki, Hitoshi Shirakawa, Adam Wahida, Bettina Proneth, Yoshiro Saito, Kiyotaka Nakagawa, Eikan Mishima, Marcus Conrad, Koya Ono, Yasutaka Kawai
|
Cell Press
Verified
Author Correction: Mechanisms controlling cellular and systemic iron homeostasis - Nature Reviews Molecular Cell Biology
Correction to: Nature Reviews Molecular Cell Biology https://doi.org/10.1038/s41580-023-00648-1, published online 2 October 2023 In the version of the article initially published, the last sentence of the “Iron transfer to the mitochondrion” section, “However, counterintuitively, MCU1 deficiency in myeloid cells leads to mitochondrial iron accumulation, not depletion”, was incorrect and so has now been removed along with the corresponding reference.
PGE2 inhibits TIL expansion by disrupting IL-2 signalling and mitochondrial function - Nature
|
Abstract Expansion of antigen-experienced CD8+ T cells is critical for the success of tumour-infiltrating lymphocyte (TIL)-adoptive cell therapy (ACT) in patients with cancer1. Interleukin-2 (IL-2) acts as a key regulator of CD8+ cytotoxic T lymphocyte functions by promoting expansion and cytotoxic capability2,3.
By Matteo Morotti, Alizée J. Grimm, Helen Hope, Marion Arnaud, David Barras, Catherine Ronet, Aspram Minasyan, Johanna Chiffelle, Fabrizio Benedetti, Riccardo Turrini, Khalil Zaman, Marcus Conrad, Lana E. Kandalaft, Julien Dagher, Jesus Corria-Osorio, Ping-Chih Ho, Alexandre Harari, Nicola Vannini, Jan P. Böttcher, Denarda Dangaj Laniti
|
Nature
Verified
Inhibition of 7-dehydrocholesterol reductase prevents hepatic ferroptosis under an active state of sterol synthesis - Nature Communications
Abstract Recent evidence indicates ferroptosis is implicated in the pathophysiology of various liver diseases; however, the organ-specific regulation mechanism is poorly understood. Here, we demonstrate 7-dehydrocholesterol reductase (DHCR7), the terminal enzyme of cholesterol biosynthesis, as a regulator of ferroptosis in hepatocytes. Genetic and pharmacological inhibition (with AY9944) of DHCR7 suppress ferroptosis in human hepatocellular carcinoma Huh-7 cells.
7-Dehydrocholesterol is an endogenous suppressor of ferroptosis - Nature
|
Abstract Ferroptosis is a form of cell death that has received considerable attention not only as a means to eradicate defined tumour entities but also because it provides unforeseen insights into the metabolic adaptation that tumours exploit to counteract phospholipid oxidation1,2. Here, we identify proferroptotic activity of 7-dehydrocholesterol reductase (DHCR7) and an unexpected prosurvival function of its substrate, 7-dehydrocholesterol (7-DHC).
By Florencio Porto Freitas, Palina Nepachalovich, Omkar Zilka, Sebastian Doll, Werner Schmitz, Ann M. Wehman, Isabel Weigand, Matthias Kroiss, Fernando Gomes, Manjima B Sathian, David B. Konrad, Douglas Covey, Ralf Bargou, Ana J. García-Sáez, Derek Pratt, Maria Fedorova, Andreas Trumpp, Marcus Conrad, Alex Inague, Karoly Mirnics
|
Nature
Verified
Mechanisms controlling cellular and systemic iron homeostasis - Nature Reviews Molecular Cell Biology
Abstract In mammals, hundreds of proteins use iron in a multitude of cellular functions, including vital processes such as mitochondrial respiration, gene regulation and DNA synthesis or repair. Highly orchestrated regulatory systems control cellular and systemic iron fluxes ensuring sufficient iron delivery to target proteins is maintained, while limiting its potentially deleterious effects in iron-mediated oxidative cell damage and ferroptosis.
Nonmetabolic role for CKB in ferroptosis - Nature Cell Biology
Cite this article Mishima, E., Conrad, M. Nonmetabolic role for CKB in ferroptosis. Nat Cell Biol 25, 633–634 (2023). https://doi.org/10.1038/s41556-023-01104-0 Download citation Published: 08 May 2023 Issue Date: May 2023 DOI: https://doi.org/10.1038/s41556-023-01104-0 Share this article Anyone you share the following link with will be able to read this content: Sorry, a shareable link is not currently available for this article.
Computational Analysis of Histamine Protonation Effects on H1R Binding
Author / Affiliation / Email Search Type Submit to this Journal Review for this Journal Edit a Special Issue Article Menu /ajax/scifeed/subscribe Altmetric share Share announcement Help format_quote Cite thumb_up ... Endorse textsms ... Comment Need Help? Support Find support for a specific problem in the support section of our website. Get Support Feedback Please let us know what you think of our products and services.
Metabolism and Cell Death
The Institute of Metabolism and Cell Death (MCD) aims to elucidate the molecular mechanisms underlying life and death decisions in (patho-)physiological contexts. Understanding these mechanisms is central to both the identification of biomarkers and the development of new therapies to combat degenerative diseases and cancer.
A non-canonical vitamin K cycle is a potent ferroptosis suppressor - Nature
Abstract Ferroptosis, a non-apoptotic form of cell death marked by iron-dependent lipid peroxidation1, has a key role in organ injury, degenerative disease and vulnerability of therapy-resistant cancers2. Although substantial progress has been made in understanding the molecular processes relevant to ferroptosis, additional cell-extrinsic and cell-intrinsic processes that determine cell sensitivity toward ferroptosis remain unknown.
Persister cancer cells: Iron addiction and vulnerability to ferroptosis
Summary Ferroptosis is a unique type of non-apoptotic cell death resulting from the unrestrained occurrence of peroxidized phospholipids, which are subject to iron-mediated production of lethal oxygen radicals. This cell death modality has been detected across many organisms, including in mammals, where it can be used as a defense mechanism against pathogens or even harnessed by T cells to sensitize tumor cells toward effective killing.
Ferroptosis: mechanisms, biology and role in disease
Abstract The research field of ferroptosis has seen exponential growth over the past few years, since the term was coined in 2012. This unique modality of cell death, driven by iron-dependent phospholipid peroxidation, is regulated by multiple cellular metabolic pathways, including redox homeostasis, iron handling, mitochondrial activity and metabolism of amino acids, lipids and sugars, in addition to various signalling pathways relevant to disease.
The Metabolic Underpinnings of Ferroptosis
Abrams R.P. Carroll W.L. Woerpel K.A. Five-membered ring peroxide selectively initiates ferroptosis in cancer cells. ACS Chem. Biol. 2016; 11: 1305-1312 Adedoyin O. Boddu R. Traylor A. Lever J.M. Bolisetty S. George J.F. Agarwal A. Heme oxygenase-1 mitigates ferroptosis in renal proximal tubule cells. Am. J. Physiol. Ren. Physiol. 2018; 314: F702-F714 Alim I. Caulfield J.T. Chen Y. Swarup V. Geschwind D.H. Ivanova E. Seravalli J. Ai Y. Sansing L.H. Ste Marie E.J. et al.
Changes in ferrous iron and glutathione promote ferroptosis and frailty in aging Caenorhabditis elegans
Abstract All eukaryotes require iron. Replication, detoxification, and a cancer-protective form of regulated cell death termed ferroptosis, all depend on iron metabolism. Ferrous iron accumulates over adult lifetime in Caenorhabditis elegans. Here, we show that glutathione depletion is coupled to ferrous iron elevation in these animals, and that both occur in late life to prime cells for ferroptosis.
Selenium: Tracing Another Essential Element of Ferroptotic Cell Death
Alim I. Caulfield J.T. Chen Y. Swarup V. Geschwind D.H. Ivanova E. Seravalli J. Ai Y. Sansing L.H. Ste Marie E.J. et al. Selenium drives a transcriptional adaptive program to block ferroptosis and treat stroke. Cell. 2019; 177: 1262-1279.e25 Altamura S. Vegi N.M. Hoppe P.S. Schroeder T. Aichler M. Walch A. Okreglicka K. Hultner L. Schneider M. Ladinig C. et al. Glutathione peroxidase 4 and vitamin E control reticulocyte maturation, stress erythropoiesis and iron homeostasis. Haematologica.
Ferroptosis at the crossroads of cancer-acquired drug resistance and immune evasion
Abstract Ferroptosis is a recently recognized cell death modality that is morphologically, biochemically and genetically distinct from other forms of cell death and that has emerged to play an important role in cancer biology. Recent discoveries have highlighted the metabolic plasticity of cancer cells and have provided intriguing insights into how metabolic rewiring is a critical event for the persistence, dedifferentiation and expansion of cancer cells.
Show More
loading
Actions
Is this you?
As a journalist, you can create a free Muck Rack account to customize your profile, list your contact preferences, and upload a portfolio of your best work.Get in touch with Marcus
Contact Marcus, search articles and posts on X, monitor coverage, and track replies from one place.
Learn more about Muck Rack