% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@MISC{Ehninger:285054,
      author       = {Ehninger, Dan and Scifo, Enzo and Morsy, Sarah},
      title        = {{D}ataset: {D}eciphering the {T}ranscriptomic {S}ignatures
                      of {A}ging {A}cross {O}rgans in {M}ice},
      publisher    = {Gene Expression Omnibus},
      reportid     = {DZNE-2026-00178},
      year         = {2026},
      abstract     = {Aging is a key risk factor for disease in mammals, yet its
                      molecular basis across organs remains unclear. Here, we
                      performed bulk RNA sequencing on eight organs (brain, heart,
                      kidney, liver, lung, skeletal muscle, spleen, testis) from
                      male C57BL/6J mice at distinct life stages. Our analysis
                      revealed that age-related transcriptomic shifts vary in
                      timing and magnitude: early in lung, spleen, testis;
                      mid-life in heart, kidney, skeletal muscle; and late in
                      brain and liver. Magnitude ranged from very low (testis),
                      low (brain, heart), moderate (lungs, skeletal muscle) to
                      high (kidneys, liver, spleen). We uncovered organ-specific
                      aging signatures, for instance, mitochondrial and epigenetic
                      regulation in the kidney, metabolic/detoxification in the
                      lung, and angiogenesis as well as ribosome biogenesis in the
                      spleen). We also identified shared transcriptomic
                      signatures, such as cellular senescence in the kidney and
                      skeletal muscle, ECM remodeling in the heart, skeletal
                      muscle and spleen), or inflammation in the heart, kidney,
                      liver and lungs. These findings highlight unique and
                      overlapping transcriptomic aging signatures, informing
                      future therapeutic strategies to improve healthspan.},
      cin          = {AG Ehninger},
      cid          = {I:(DE-2719)1013005},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)32},
      url          = {https://pub.dzne.de/record/285054},
}