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RESEARCH PAPER / 2026-02-13

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

Veronica Bergo, Pavlos Bousounis, Giang To Vu, Mélodie Douté, Aikaterini Polyzou, Maria-Eleni Lalioti, Bogdan B Grigorash, Lyudmila Tsurkan, Nicholas Morchel, Ward Deboutte, Frédéric Brau, Thomas Manke, Hind Medyouf, Dmitry V Bulavin, Nina Cabezas-Wallscheid, Marta Derecka, Eirini Trompouki

Max Planck Institute of Immunobiology and Epigenetics, Freiburg, Germany. [email protected] Planck Institute of Immunobiology and Epigenetics, Freiburg, Germany. [email protected]. · pubmed

Abstract

"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

The following analysis is generated by AI and may contain errors. It is separate from the authors’ abstract and is not peer review.

Research summary

The paper claims that the lack of MDA5 delays hematopoietic aging by modulating inflammaging and proteostasis in mice. This research addresses the mechanisms underlying hematopoietic aging, which is a fundamental aspect of the aging process and could contribute to understanding and potentially mitigating age-related decline.

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