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Lack of MDA5 delays hematopoietic aging by modulating inflammaging and proteostasis in mice

Title: Lack of MDA5 delays hematopoietic aging by modulating inflammaging and proteostasis in mice
Authors: Bergo, Veronica; Bousounis, Pavlos; To Vu, Giang; Douté, Mélodie; Polyzou, Aikaterini; Lalioti, Maria-Eleni; Grigorash, Bogdan B.; Tsurkan, Lyudmila; Morchel, Nicholas; Deboutte, Ward; Brau, Frédéric; Manke, Thomas; Sagar; Medyouf, Hind; Bulavin, Dmitry V.; Cabezas Wallscheid, Nina; id_orcid:0 000-0003-0870-0530; Derecka, Marta; Trompouki, Eirini
Source: Nature Communications, 17 (1)
Publisher Information: Nature
Publication Year: 2026
Collection: ETH Zürich Research Collection
Description: “Inflammaging”, the chronic increase in inflammatory signaling with age, remains poorly understood in hematopoietic aging. Here, we identify the innate immune RNA sensor melanoma differentiation–associated protein 5 (MDA5) as an important factor of hematopoietic stem cell (HSC) aging. Aged Mda5 -/- mice exhibit reduced HSC accumulation and myeloid bias. Importantly, aged Mda5 -/- HSCs retain greater quiescence and superior repopulation capacity in noncompetitive transplants compared to wild-type counterparts. Multiomic analyses— including chromatin accessibility, transcriptomics, and metabolomics—reveal decreased inflammatory signaling, a youthful metabolic profile, and improved proteostasis in Mda5 -/- HSCs, through regulation of HSF1 and phospho-EIF2A, key proteostasis regulators. Activation of HSF1 in aged wild-type HSCs partially restores youthful features, supporting a causal role for proteostasis maintenance. Collectively, our findings demonstrate that attenuating MDA5-dependent inflammation preserves HSC function during aging by maintaining metabolic fitness and proteostasis and provide insight into potential therapeutic strategies for mitigating hematopoietic aging. ; ISSN:2041-1723
Document Type: article in journal/newspaper
File Description: application/application/pdf
Language: English
Relation: info:eu-repo/semantics/altIdentifier/wos/001689721200002; https://hdl.handle.net/20.500.11850/796151
DOI: 10.3929/ethz-c-000796151
Availability: https://hdl.handle.net/20.500.11850/796151; https://doi.org/10.3929/ethz-c-000796151
Rights: info:eu-repo/semantics/openAccess ; http://creativecommons.org/licenses/by/4.0/ ; Creative Commons Attribution 4.0 International
Accession Number: edsbas.A5E77481
Database: BASE