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@ARTICLE{Drekolia:305605,
      author       = {M.-K. Drekolia and J. Mettner and D. Wang and F. Delgado
                      Lagos and C. Koch and D. Hecker and J. Eresch and Y. Mao and
                      M. Bähr$^*$ and D. Weichenhan$^*$ and J. Cordero and J.
                      Wittig and B. Zhang and H. Cui and X. Li and J. A. Oo and A.
                      Weigert and M. Siragusa and S. Klatt and I. Fleming and S.
                      Günther and M. Looso and R. P. Brandes and H. F. Langer and
                      A. Papapetropoulos and M. Singhal and M. H. Schulz and C.
                      Plass$^*$ and J. Heineke and G. Dobreva and J. Hu and S.-I.
                      Bibli},
      title        = {{C}ystine import and oxidative catabolism fuel vascular
                      growth and repair via nutrient-responsive histone
                      acetylation.},
      journal      = {Cell metabolism},
      volume       = {nn},
      issn         = {1550-4131},
      address      = {Amsterdam [u.a.]},
      publisher    = {Elsevier},
      reportid     = {DKFZ-2025-02255},
      pages        = {nn},
      year         = {2025},
      note         = {epub},
      abstract     = {Endothelial metabolism underpins tissue regeneration,
                      health, and longevity. We uncover a nuclear oxidative
                      catabolic pathway linking cystine to gene regulation. Cells
                      preparing to proliferate upregulate the SLC7A11 transporter
                      to import cystine, which is oxidatively catabolized by
                      cystathionine-γ-lyase (CSE) in the nucleus. This generates
                      acetyl units via pyruvate dehydrogenase, driving
                      site-specific histone H3 acetylation and chromatin
                      remodeling that sustain endothelial transcription and
                      proliferation. Combined loss of SLC7A11 and CSE abolishes
                      cystine oxidative and reductive metabolism and causes
                      embryonic lethality, whereas single deletions reveal
                      distinct effects. SLC7A11 deficiency triggers compensatory
                      cysteine de novo biosynthesis, partially maintaining
                      angiogenesis, while CSE deletion disrupts nuclear cystine
                      oxidative catabolism, transcription, and vessel formation.
                      Therapeutically, cystine supplementation promotes vascular
                      repair in retinopathy of prematurity, myocardial infarction,
                      and injury in aging. These findings establish the role of
                      cystine nuclear oxidative catabolism as a fundamental
                      metabolic axis coupling nutrient utilization to gene
                      regulation, with implications for vascular regeneration.},
      keywords     = {CSE (Other) / SLC7A11 (Other) / aging (Other) / cystine
                      (Other) / epigenetics (Other) / vascular growth (Other)},
      cin          = {B370},
      ddc          = {570},
      cid          = {I:(DE-He78)B370-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41175867},
      doi          = {10.1016/j.cmet.2025.10.003},
      url          = {https://inrepo02.dkfz.de/record/305605},
}