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@ARTICLE{Morsy:283153,
      author       = {Morsy, Sarah and Scifo, Enzo and Xie, Kan and Schaaf,
                      Kristina and Russ, Jenny and Paulusch, Stefan and De
                      Domenico, Elena and Salomoni, Paolo and Bano, Daniele and
                      Ehninger, Dan},
      title        = {{D}eciphering the {T}ranscriptomic {S}ignatures of {A}ging
                      {A}cross {O}rgans in {M}ice},
      journal      = {Aging cell},
      volume       = {25},
      number       = {2},
      issn         = {1474-9718},
      address      = {Oxford [u.a.]},
      publisher    = {Wiley-Blackwell},
      reportid     = {DZNE-2026-00049},
      pages        = {e70357},
      year         = {2026},
      abstract     = {Aging, a major risk factor for numerous diseases, is
                      associated with significant transcriptional changes across
                      organs. However, the age of onset, extent of transcriptomic
                      changes and how they unfold are not fully understood. We
                      performed bulk RNA sequencing on eight organs (brain, heart,
                      kidney, liver, lung, skeletal muscle, spleen, and testis)
                      from male C57BL/6J mice across much of the murine lifespan
                      covering 3-, 5-, 8-, 14-, 20- and 26-month-old animals. Our
                      analysis revealed that age-related transcriptomic shifts
                      vary in both timing and extent, with early shifts in lung,
                      spleen, and testis; mid-life changes in heart, kidney, and
                      skeletal muscle; and later alterations in brain and liver.
                      The extent of age-related transcriptomic changes ranged from
                      very low (testis) to high (kidney, liver, spleen). A linear
                      mixed-effects model identified genes with tissue-specific
                      aging trajectories. By integrating hub gene analysis and
                      functional enrichment, we uncovered aging signatures that
                      are either tissue-specific or shared across multiple organs,
                      including those related to immune response, mitochondrial
                      dysfunction, extracellular matrix remodeling, and cellular
                      senescence. This study provides a systems-level resource for
                      advancing aging research.},
      cin          = {AG Ehninger / AG Salomoni / AG Schultze / PRECISE / AG
                      Bano},
      ddc          = {610},
      cid          = {I:(DE-2719)1013005 / I:(DE-2719)1013032 /
                      I:(DE-2719)1013038 / I:(DE-2719)1013031 /
                      I:(DE-2719)1013003},
      pnm          = {352 - Disease Mechanisms (POF4-352) / 354 - Disease
                      Prevention and Healthy Aging (POF4-354) / 351 - Brain
                      Function (POF4-351)},
      pid          = {G:(DE-HGF)POF4-352 / G:(DE-HGF)POF4-354 /
                      G:(DE-HGF)POF4-351},
      experiment   = {EXP:(DE-2719)PRECISE-20190321},
      typ          = {PUB:(DE-HGF)16},
      doi          = {10.1111/acel.70357},
      url          = {https://pub.dzne.de/record/283153},
}