MCD

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.

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Kidney tubular cells dying by ferroptosis

We are convinced that a detailed mechanistic understanding of the molecular mechanisms underlying metabolic cell death or leaving a vulnerability to these forms of cell death will provide us unique opportunities to combat these often fatal diseases.

We are interested in understanding how mitochondrial metabolic plasticity paves the way for cells to adapt to stress and how this knowledge can help address diseases like neurodegeneration and mitochondrial disorders.

The cornerstone of our research is to identify ferroptotic signatures in pathological conditions relevant to ferroptosis with potential for biomarker development using (oxi-)lipidomic and metabolomic workflows.

Ferroptotic cell death is thought to be the root cause of many degenerative diseases while ferroptosis suppression has been put forward as Achilles’ heel for therapy-resistant tumors. Ferroptosis modulators have a vast potential for the treatment of as-yet-incurable diseases

The management and analysis of increasingly large amounts of research data is of enormous importance for the understanding of fundamental metabolic processes, their regulation and the subsequent development of innovative approaches to disease therapy.

Ferroptosis: from Molecular Basics to Clinical Applications

Regulation of Cell Death Decisions

Irondeath

Porträt Marcus Conrad
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Prof. Marcus Conrad, Director of the Institute of Metabolism and Cell Death at Helmholtz Munich was awarded the German Cancer Award 2026 in the category “Experimental Research”, together with Prof. José Pedro Friedmann Angeli of the University of…

Bloodstream Flow 3D Render of Red Blood Cells in Vessel Lumen

Research into a novel form of cell death is entering its next phase and could soon help reduce complications after heart attacks or organ transplants. The Federal Ministry of Research, Technology, and Space (BMFTR) is providing continued support for…

Researchers at Helmholtz Munich, the Technical University of Munich and the LMU University Hospital Munich uncovered a mechanism that protects nerve cells from premature cell death, known as ferroptosis. The study provides the first molecular…

Two new studies published in Nature show that metastatic melanoma and lung adenocarcinoma rely on the protein ferroptosis suppressor protein 1 (FSP1) for survival – identifying a metabolic dependency that may inform the development of new cancer…

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Researchers at Helmholtz Munich have secured three prestigious Proof of Concept Grants from the European Research Council (ERC). This funding will enable them to advance innovative projects across diverse areas of biomedical research. With a total of…

For his discoveries in the field of ferroptosis – a specific form of programmed cell death that opens up new perspectives for the development of drugs in cancer therapy and organ transplantation – Prof. Marcus Conrad has been awarded the Paul Martini…

Ferroptosis: when metabolism meets cell death

Exploiting ferroptosis vulnerabilities in cancer

Ferroptosis – Chains of Death

PRDX6 dictates ferroptosis sensitivity by directing cellular selenium utilization

Phase separation of FSP1 promotes ferroptosis

Porträt Marcus Conrad_KI_Erweiterung für Typo3

Marcus Conrad is listed as one of the most influential scientists for five years in a row

Prof. Dr. Marcus Conrad

Director Metabolism and Cell Death, MCD

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Dr. Bettina Proneth

Deputy Director

Dr. Jens Hansen

Group Leader

Dr. Maceler Aldrovandi

Group Leader

Dr. Sebastian Doll

Group Leader

Dr. Soni Deshwal

Group Leader, MCD

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Kawamura, K. ; Ono, K. ; Mishima, E. ; Hashizume, O. ; Conrad, M. ; Miki, H. ; Funato, Y.

Cellular Mg²⁺ decrease causes a distinctive NF-κB-dependent form of cell death.

Takashima, H. ; Makino, R. ; Taguchi, H. ; Ito, J. ; Mishima, E. ; Takenaka, Y. ; Akiyama, Y. ; Sumi, D. ; Conrad, M. ; Tomikoka, Y. ; Toyama, T. ; Saito, Y.

Arsenite sensitizes to ferroptosis by disrupting selenium metabolism and reducing GPx4 expression.

Tonnus, W. ; Maremonti, F. ; Gavali, S. ; Schlecht, M.N. ; Gembardt, F. ; Belavgeni, A. ; Leinung, N. ; Flade, K. ; Bethe, N. ; Traikov, S. ; Haag, A. ; Schilling, D. ; Penkov, S. ; Mallais, M. ; Gaillet, C. ; Meyer, C. ; Katebi, M. ; Ray, A. ; Gerhardt, L.M.S. ; Brucker, A. ; Becker, J.N. ; Tmava, M. ; Schlicker, L. ; Schulze, A. ; Himmerkus, N. ; Shevchenko, A. ; Peitzsch, M. ; Barayeu, U. ; Nasi, S. ; Putz, J. ; Korach, K.S. ; Neugarten, J. ; Golestaneh, L. ; Hugo, C. ; Becker, J.U. ; Weinberg, J.M. ; Lorenz, S. ; Proneth, B. ; Conrad, M. ; Wolf, E. ; Plietker, B. ; Rodriguez, R. ; Pratt, D.A. ; Dick, T.P. ; Fedorova, M. ; Bornstein, S.R. ; Linkermann, A.

Publisher Correction: Multiple oestradiol functions inhibit ferroptosis and acute kidney injury.

Lorenz, S. ; Wahida, A. ; Bostock, M.J. ; Seibt, T. ; Santos Dias Mourão, A. ; Levkina, A. ; Trümbach, D. ; Soudy, M. ; Emler, D. ; Rothammer, N. ; Woo, M.S. ; Sonner, J.K. ; Novikova, M. ; Henkelmann, B. ; Aldrovandi, M. ; Kaemena, D.F. ; Mishima, E. ; Vermonden, P. ; Zong, Z. ; Cheng, D. ; Nakamura, T. ; Ito, J. ; Doll, S. ; Proneth, B. ; Bürkle, E. ; Rizzollo, F. ; Escamilla Ayala, A. ; Napolitano, V. ; Kolonko, M. ; Gaussmann, S. ; Merl-Pham, J. ; Hauck, S.M. ; Pertek, A. ; Orschmann, T. ; Van San, E. ; Vanden Berghe, T. ; Hass, D, ; Maida, A. ; Frenz, J.M. ; Pedrera, L. ; Dolga, A.M. ; Kraiger, M. ; Hrabě de Angelis, M. ; Fuchs, H. ; Ebert, G. ; Lenberg, J. ; Friedman, J. ; Scale, C. ; Agostinis, P. ; Zimprich, A. ; Vogt Weisenhorn, D.M. ; Garrett, L. ; Hölter, S.M. ; Wurst, W. ; Glaab, E. ; Lewerenz, J. ; Popper, B. ; Sieben, C. ; Steinacker, P. ; Zischka, H. ; García-Sáez, A.J. ; Tietze, A. ; Ramesh, S.K. ; Ayton, S. ; Vincendeau, M. ; Friese, M.A. ; Wigby, K. ; Sattler, M. ; Mann, M. ; Ingold, I. ; Jayavelu, A.K. ; Popowicz, G.M. ; Conrad, M.

A fin-loop-like structure in GPX4 underlies neuroprotection from ferroptosis.

Wu, K. ; Vaughan, A.J. ; Bossowski, J.P. ; Hao, Y. ; Ziogou, A. ; Kim, S.M. ; Kim, T.H. ; Nakamura, M.N. ; Pillai, R. ; Mancini, M. ; Rajalingam, S. ; Han, M. ; Nakamura, T. ; Wang, L. ; Chung, S.J. ; Simeone, D. ; Shackelford, D. ; Kang, Y.P. ; Conrad, M. ; Papagiannakopoulos, T.

Targeting FSP1 triggers ferroptosis in lung cancer.

Palma, M. ; Chaufan, M. ; Breuer, C.B. ; Müller, S. ; Sabatier, M. ; Fraser, C.S. ; Szylo, K.J. ; Yavari, M. ; Carmona, A. ; Kaur, M. ; Melo, L.M.N. ; Cansiz, F. ; Monge-Lorenzo, J. ; Flores, M.A.E. ; Mishima, E. ; Nakamura, T. ; Proneth, B. ; Labrado, M. ; Liang, Y. ; Cayting, N. ; Zheng, L. ; Cañeque, T. ; Colombeau, L. ; Wahida, A. ; Friedmann Angeli, J.P. ; Tasdogan, A. ; Hui, S.T. ; Rodriguez, R. ; Conrad, M. ; Reticker-Flynn, N.E. ; Ubellacker, J.M.

Lymph node environment drives FSP1 targetability in metastasizing melanoma.

Vandenabeele, P. ; Conrad, M. ; Wahida, A.

For better or worse: The impact of necrotic cell death modalities.