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@ARTICLE{Li:298414,
      author       = {S. Li and H. Li$^*$ and K. Bennewitz and G. Poschet and M.
                      Buettner and I. Hausser and J. Szendroedi and P. P. Nawroth
                      and J. Kroll},
      title        = {{C}ombined loss of glyoxalase 1 and aldehyde dehydrogenase
                      3a1 amplifies dicarbonyl stress, impairs proteasome activity
                      resulting in hyperglycemia and activated retinal
                      angiogenesis.},
      journal      = {Metabolism},
      volume       = {165},
      issn         = {0026-0495},
      address      = {Orlando, Fla.},
      publisher    = {Elsevier},
      reportid     = {DKFZ-2025-00270},
      pages        = {156149},
      year         = {2025},
      note         = {2025 Apr;165:156149},
      abstract     = {Any energy consumption results in the generation of highly
                      reactive dicarbonyls and the need to prevent excessive
                      dicarbonyls accumulation through the activity of several
                      interdependent detoxification enzymes. Glyoxalase 1 (GLO1)
                      knockout zebrafish showed only moderately elevated
                      methylglyoxal (MG) levels, but increased Aldehyde
                      Dehydrogenases (ALDH) activity and increased aldh3a1
                      expression. Elevated levels of 4-hydroxynonenal (4-HNE) but
                      no MG increase were observed in ALDH3A1KO. The question of
                      whether ALDH3A1 prevents MG formation as a compensatory
                      mechanism in the absence of GLO1 remained unclear.To
                      investigate whether ALDH3A1 detoxifies MG as a compensatory
                      mechanism in the absence of GLO1, the GLO1/ALDH3A1 double
                      knockout (DKO) zebrafish was first generated. Various
                      metabolites including advanced glycation end products
                      (AGEs), as well as glucose metabolism and hyaloid
                      vasculature were analyzed in GLO1KO, ALDH3A1KO and
                      GLO1/ALDH3A1DKO zebrafish.In the absence of GLO1 and
                      ALDH3A1, MG-H1 levels were increased. MG-H1 accumulation led
                      to a severe deterioration of proteasome function, resulting
                      in impaired glucose homeostasis and consequently amplified
                      angiogenic activation of the hyaloid and retinal
                      vasculature. Rescue of these pathological processes could be
                      observed by using L-carnosine, and proteasome activator
                      betulinic acid.The present data, together with previous
                      studies, suggest that ALDH3A1 and GLO1 are important
                      detoxification enzymes that prevent the deleterious effects
                      of MG-H1 accumulation on proteasome function, glucose
                      homeostasis and vascular function.},
      keywords     = {ALDH3A1 (Other) / Diabetes (Other) / Diabetic retinopathy
                      (Other) / Dicarbonyl stress (Other) / GLO1 (Other) /
                      MG-derived hydroimidazolone 1 (MG-H1) (Other) / Proteasome
                      dysfunction (Other) / Zebrafish (Other)},
      cin          = {D400},
      ddc          = {610},
      cid          = {I:(DE-He78)D400-20160331},
      pnm          = {314 - Immunologie und Krebs (POF4-314)},
      pid          = {G:(DE-HGF)POF4-314},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:39892865},
      doi          = {10.1016/j.metabol.2025.156149},
      url          = {https://inrepo02.dkfz.de/record/298414},
}