Targeting NLRP3 inhibits AML progression by inducing PERK/eIF2-mediated apoptosis

Our findings elucidate the involvement of the NLRP3/PERK/eIF2 axis as a novel driver of AML cell survival. Targeting NLRP3-induced signaling pathways, particularly through the PERK/eIF2 axis, presents a promising therapeutic strategy for AML intervention. These insights into the role of the NLRP3 inflammasome offer potential avenues for improving the prognosis and treatment outcomes of AML patients.

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Publication Details

Journal
Cell Communication and Signaling
Published
2024-09-02
DOI
https://doi.org/10.1186/s12964-024-01777-6
Citations
8
Primary Topic
Inflammasome and immune disorders
Type
article
Field-Weighted Citation Impact
1.87

Funders

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article

Targeting NLRP3 inhibits AML progression by inducing PERK/eIF2-mediated apoptosis

Daniel Neureiter, Dirk Schmidt‐Arras, Michael Stefan Unger, Philip Steiner et al.
8 citations
Cell Communication and Signaling
Inflammasome and immune disorders
1.87
article

Targeting NLRP3 inhibits AML progression by inducing PERK/eIF2-mediated apoptosis

Daniel Neureiter, Dirk Schmidt‐Arras, Michael Stefan Unger, Philip Steiner, Julia Vetter, Dirk Strunk, Richard Greil, Fritz Aberger, Helene Sieberer, Susanne Schaller, Helen Strandt, Constantin Blöchl, Stephan Winkler, Tanja Nicole Hartmann, Christian X. Weichenberger, Lisa Pleyer, Jutta Horejs‐Hoeck, Ancuela Andosch, Suzana Tesanovic, Theresa Neuper, Diana Amend, Dominik P. Elmer, Hieu-Hoa Dang, Michela Luciano, Peter W. Krenn, Christian G. Huber, Anna Eglseer, Laura Hummer, Stephanie Binder, Renate Bauer
article en
8 citations

Abstract

Our findings elucidate the involvement of the NLRP3/PERK/eIF2 axis as a novel driver of AML cell survival. Targeting NLRP3-induced signaling pathways, particularly through the PERK/eIF2 axis, presents a promising therapeutic strategy for AML intervention. These insights into the role of the NLRP3 inflammasome offer potential avenues for improving the prognosis and treatment outcomes of AML patients.

Cell Communication and SignalingVol. 22(1)
Johannes Kepler University of Linz (AT), Eurac Research (IT), University of Freiburg (DE), University of Salzburg (AT), Paracelsus Medical University (AT), University Medical Center Freiburg (DE), Institute for Biomedicine (IT), University of Applied Sciences Upper Austria (AT), Unfallkrankenhaus Salzburg (AT)
Austrian Science Fund, Universität Salzburg, José Carreras Leukämie-Stiftung, Salzburger Landesregierung, Interreg
Good health and well-being
Openalex Percentile: Top 14%
Inflammasome and immune disorders
1.87
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