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@ARTICLE{Gisa:279375,
      author       = {Gisa, Verena and Islam, Md Rezaul and Lbik, Dawid and
                      Hofmann, Raoul Maximilian and Pena, Tonatiuh and Krüger,
                      Dennis Manfred and Burkhardt, Susanne and Schütz, Anna-Lena
                      and Sananbenesi, Farahnaz and Toischer, Karl and Fischer,
                      Andre},
      title        = {{R}ole of {C}ompensatory mi{RNA} {N}etworks in {C}ognitive
                      {R}ecovery from {H}eart {F}ailure.},
      journal      = {Non-Coding RNA},
      volume       = {11},
      number       = {3},
      issn         = {2311-553X},
      address      = {Basel},
      publisher    = {MDPI},
      reportid     = {DZNE-2025-00752},
      pages        = {45},
      year         = {2025},
      abstract     = {Background: Heart failure (HF) is associated with an
                      increased risk of cognitive impairment and hippocampal
                      dysfunction, yet the underlying molecular mechanisms remain
                      poorly understood. This study aims to investigate the role
                      of microRNA (miRNA) networks in hippocampus-dependent memory
                      recovery in a mouse model of HF. Methods: CaMKIIδC
                      transgenic (TG) mice, a model for HF, were used to assess
                      hippocampal function at 3 and 6 months of age. Memory
                      performance was evaluated using hippocampus-dependent
                      behavioral tasks. Small RNA sequencing was performed to
                      analyze hippocampal miRNA expression profiles across both
                      time points. Bioinformatic analyses identified miRNAs that
                      potentially regulate genes previously implicated in
                      HF-induced cognitive impairment. Results: We have previously
                      shown that at 3 months of age, CaMKIIδC TG mice exhibited
                      significant memory deficits associated with dysregulated
                      hippocampal gene expression. In this study, we showed that
                      these impairments, memory impairment and hippocampal gene
                      expression, were no longer detectable at 6 months, despite
                      persistent cardiac dysfunction. However, small RNA
                      sequencing revealed a dynamic shift in hippocampal miRNA
                      expression, identifying 27 miRNAs as 'compensatory miRs'
                      that targeted $73\%$ of the transcripts dysregulated at 3
                      months but reinstated by 6 months. Notably, miR-181a-5p
                      emerged as a central regulatory hub, with its downregulation
                      coinciding with restored memory function. Conclusions: These
                      findings suggest that miRNA networks contribute to the
                      restoration of hippocampal function in HF despite continued
                      cardiac pathology and provide an important compensatory
                      mechanism towards memory impairment. A better understanding
                      of these compensatory miRNA mechanisms may provide novel
                      therapeutic targets for managing HF-related cognitive
                      dysfunction.},
      keywords     = {Alzheimer (Other) / MicroRNA (Other) / cognitive impairment
                      (Other) / heart failure (Other) / hippocampal function
                      (Other) / memory recovery (Other) / transcriptional
                      homeostasis (Other)},
      cin          = {AG Fischer / Bioinformatics Unit (Göttingen) / AG
                      Sananbenesi},
      ddc          = {570},
      cid          = {I:(DE-2719)1410002 / I:(DE-2719)1440016 /
                      I:(DE-2719)1410004},
      pnm          = {352 - Disease Mechanisms (POF4-352) / 899 - ohne Topic
                      (POF4-899)},
      pid          = {G:(DE-HGF)POF4-352 / G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40559623},
      pmc          = {pmc:PMC12196295},
      doi          = {10.3390/ncrna11030045},
      url          = {https://pub.dzne.de/record/279375},
}