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REVIEW article
Front. Cell Dev. Biol.
Sec. Cellular Biochemistry
Volume 13 - 2025 | doi: 10.3389/fcell.2025.1564649
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Recent studies have investigated the key roles exerted by ERAP1 and ERAP2 in maintaining cellular homeostasis, emphasizing their functions beyond traditional antigen processing and presentation. In particular, genetic variants of these IFNγ-inducible aminopeptidases significantly impact critical cellular pathways, including migration, angiogenesis, and autophagy, which are essential in immune responses and disease processes. ERAP1's influence on endothelial cell migration and VEGF-driven angiogenesis, along with ERAP2's role in managing stress-induced autophagy via the UPR, highlights their importance in cellular adaptation to stress and disease outcomes, including autoimmune diseases, cancer progression, and infections. By presenting recent insights into ERAP1 and ERAP2 functions, this review underscores their potential as therapeutic targets in immune regulation and cellular stress-response pathways.
Keywords: ERAPs, Cell Biology, cell migration, er stress, Autopaghy
Received: 21 Jan 2025; Accepted: 12 Mar 2025.
Copyright: © 2025 Saulle, Vitalyos, D'Agate, Clerici and Biasin. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Mara Biasin, University of Milan, Milan, Italy
Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.
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