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@ARTICLE{Piazzesi:163786,
      author       = {Piazzesi, Antonia and Wang, Yiru and Jackson, Joshua and
                      Wischhof, Lena and Zeisler-Diehl, Viktoria and Scifo, Enzo
                      and Oganezova, Ina and Hoffmann, Nils Thorben and Gomez,
                      Pablo and Bertan, Fabio and Wrobel, Chester J J and
                      Schroeder, Frank C and Ehninger, Dan and Händler, Kristian
                      and Schultze, Joachim L and Schreiber, Lukas and
                      Echten-Deckert, Gerhild and Nicotera, Pierluigi and Bano,
                      Daniele},
      title        = {{CEST}‐2.2 overexpression alters lipid metabolism and
                      extends longevity of mitochondrial mutants},
      journal      = {EMBO reports},
      volume       = {23},
      number       = {5},
      issn         = {1469-221X},
      address      = {Hoboken, NJ [u.a.]},
      publisher    = {Wiley},
      reportid     = {DZNE-2022-00524},
      pages        = {e52606},
      year         = {2022},
      abstract     = {Mitochondrial dysfunction can either extend or decrease
                      Caenorhabditis elegans lifespan, depending on whether
                      transcriptionally regulated responses can elicit durable
                      stress adaptation to otherwise detrimental lesions. Here, we
                      test the hypothesis that enhanced metabolic flexibility is
                      sufficient to circumvent bioenergetic abnormalities
                      associated with the phenotypic threshold effect, thereby
                      transforming short-lived mitochondrial mutants into
                      long-lived ones. We find that CEST-2.2, a carboxylesterase
                      mainly localizes in the intestine, may stimulate the
                      survival of mitochondrial deficient animals. We report that
                      genetic manipulation of cest-2.2 expression has a minor
                      lifespan impact on wild-type nematodes, whereas its
                      overexpression markedly extends the lifespan of complex
                      I-deficient gas-1(fc21) mutants. We profile the
                      transcriptome and lipidome of cest-2.2 overexpressing
                      animals and show that CEST-2.2 stimulates lipid metabolism
                      and fatty acid beta-oxidation, thereby enhancing
                      mitochondrial respiratory capacity through complex II and
                      LET-721/ETFDH, despite the inherited genetic lesion of
                      complex I. Together, our findings unveil a metabolic pathway
                      that, through the tissue-specific mobilization of lipid
                      deposits, may influence the longevity of mitochondrial
                      mutant C. elegans.},
      keywords     = {Animals / Caenorhabditis elegans: metabolism /
                      Caenorhabditis elegans Proteins: genetics / Caenorhabditis
                      elegans Proteins: metabolism / Lipid Metabolism: genetics /
                      Longevity: genetics / Mitochondria: metabolism},
      cin          = {AG Bano / AG Ehninger / AG Schultze / $R\&D$ PRECISE /
                      Scientific board},
      ddc          = {570},
      cid          = {I:(DE-2719)1013003 / I:(DE-2719)1013005 /
                      I:(DE-2719)1013031 / I:(DE-2719)5000031 /
                      I:(DE-2719)1030000},
      pnm          = {351 - Brain Function (POF4-351) / 352 - Disease Mechanisms
                      (POF4-352) / 354 - Disease Prevention and Healthy Aging
                      (POF4-354)},
      pid          = {G:(DE-HGF)POF4-351 / G:(DE-HGF)POF4-352 /
                      G:(DE-HGF)POF4-354},
      typ          = {PUB:(DE-HGF)16},
      pmc          = {pmc:PMC9066074},
      pubmed       = {pmid:35297148},
      doi          = {10.15252/embr.202152606},
      url          = {https://pub.dzne.de/record/163786},
}