Authors: Li-Li Bao, Yu-Qiang Yu, Miguel González-Acera, Jay V. Patankar, Andreas Giessl, Gregor Sturm, Anja A. Kühl, Raja Atreya, Lena Erkert, Reyes Gámez-Belmonte, Susanne M. Krug, Benjamin Schmid, Philipp Tripal, Mircea T. Chiriac, Kai Hildner, Britta Siegmund, Stefan Wirtz, Michael Stürzl, Mariam Mohamed Abdou, Zlatko Trajanoski, , Markus F. Neurath, Antonio Zorzano, Christoph Becker, Imke Atreya, Petra Bacher, Christian Bojarski, Nathalie Britzen-Laurent, Caroline Bosch-Voskens, Hyun-Dong Chang, Andreas Diefenbach, Claudia Günther, Ahmed N. Hegazy, Christoph S. N. Klose, Kristina Koop, Moritz Leppkes, Rocío López-Posadas, Leif S.-H. Ludwig, Clemens Neufert, Christina Plattner, Magdalena Prüß, Andreas Radbruch, Chiara Romagnani, Francesca Ronchi, Ashley Sanders, Alexander Scheffold, Jörg-Dieter Schulzke, Michael Schumann, Sebastian Schürmann, Antigoni Triantafyllopoulou, Maximilian Waldner, Carl Weidinger, Sebastian Zundler
Published: 2025-01-15
DOI: 10.1126/scitranslmed.adn8699
Source: Full article
Dysregulation at the intestinal epithelial barrier is a driver of inflammatory bowel disease (IBD). However, the molecular mechanisms of barrier failure are not well understood. Here, we demonstrate dysregulated mitochondrial fusion in intestinal epithelial cells (IECs) of patients with IBD and show that impaired fusion is sufficient to drive chronic intestinal inflammation. We found reduced expression of mitochondrial fusion–related genes, such as the dynamin-related guanosine triphosphatase (GTPase) optic atrophy 1 (