JAK1/2 inhibitor ruxolitinib reduces aggregates in cardiac proteinopathy
aggregate load and prevented cardiac dysfunction in DRM mice. Similar findings were obtained by crossing DRM mice with the cardiomyocyte-specific Jak1 knockout, suggesting JAK1 as a therapeutic target in proteinopathy.
Authors
- Jeffrey Robbins (ORCID: https://orcid.org/0000-0002-3345-5226)
- Moritz Meyer-Jens (ORCID: https://orcid.org/0000-0002-2922-0950)
- Ellen Orthey
- Erda Alizoti (ORCID: https://orcid.org/0009-0007-4448-3189)
- Christian Conze (ORCID: https://orcid.org/0000-0002-8849-1064)
- Leonie Ewald
- Simona Parretta
- Lucie Carrier
- Jacob J K March
- Sonia R Singh
Institutions
- Cincinnati Children's Hospital Medical Center (US)
- Universität Hamburg (DE)
- Leibniz Association (DE)
- University Medical Center Hamburg-Eppendorf (DE)
- German Centre for Cardiovascular Research (DE)
Publication Details
- Journal
- EMBO Molecular Medicine
- Published
- 2026-03-31
- DOI
- https://doi.org/10.1038/s44321-026-00411-x
- Primary Topic
- Skin and Cellular Biology Research
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- Deutsches Zentrum für Herz-Kreislaufforschung
- Fondation Leducq