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@ARTICLE{Sedda:303062,
      author       = {F. Sedda and A. Caddeo and K. Sasidharan and G. Perra and
                      R. Pal$^*$ and N. Lai and M. A. Kowalik and A. Perra},
      title        = {{G}alectin-3 inhibition ameliorates hepatic steatosis in a
                      multilineage 3{D} spheroid model.},
      journal      = {PLOS ONE},
      volume       = {20},
      number       = {7},
      issn         = {1932-6203},
      address      = {San Francisco, California, US},
      publisher    = {PLOS},
      reportid     = {DKFZ-2025-01492},
      pages        = {e0326373 -},
      year         = {2025},
      abstract     = {Metabolic dysfunction-associated steatotic liver disease
                      (MASLD) is the leading cause of chronic liver disease, and
                      liver-related morbidity and mortality worldwide. MASLD is a
                      multifactorial condition, which still needs to be completely
                      understood. Galectin 3 (Gal-3) is up-regulated in several
                      liver disorders suggesting its implication in the mechanisms
                      underlying liver damage.A human multilineage 3D model was
                      utilized to investigate the role of Gal-3 in MASLD
                      development. Human hepatoma cell line (HepG2) and human
                      stellate cell line (LX-2) were co-cultured in a
                      physiological ratio of 24:1 and treated with a mixture of
                      palmitic and oleic acid (PAOA, ratio 1:2) to induce
                      hepatocyte steatosis and facilitate the development of
                      fibrosis. While the effect of LGALS3 silencing on neutral
                      fat content was assessed by Oil-Red-O (ORO) staining, type I
                      collagen production was analysed by immunofluorescent
                      staining for collagen type I alpha 1 (COL1A1).Gal-3
                      depletion caused a reduction of neutral lipid content and
                      COL1A1 accumulation in 3D spheroids. While LGALS3 silencing
                      did not significantly alter the respiratory state, analysis
                      of genes involved in lipid metabolism demonstrated
                      significant changes in genes involved in β-oxidation and
                      triglyceride synthesis.These results suggest a role of Gal-3
                      in the regulation of fatty acid and collagen accumulation,
                      thereby indicating that approaches aimed at inhibiting Gal-3
                      may represent a promising therapeutic strategy in MASLD.},
      keywords     = {Humans / Galectin 3: antagonists $\&$ inhibitors / Galectin
                      3: metabolism / Galectin 3: genetics / Spheroids, Cellular:
                      metabolism / Spheroids, Cellular: pathology / Spheroids,
                      Cellular: drug effects / Fatty Liver: metabolism / Fatty
                      Liver: pathology / Fatty Liver: genetics / Hep G2 Cells /
                      Lipid Metabolism: genetics / Collagen Type I: metabolism /
                      Hepatocytes: metabolism / Hepatic Stellate Cells: metabolism
                      / Hepatic Stellate Cells: pathology / Blood Proteins /
                      Galectins / Galectin 3 (NLM Chemicals) / LGALS3 protein,
                      human (NLM Chemicals) / Collagen Type I (NLM Chemicals) /
                      Blood Proteins (NLM Chemicals) / Galectins (NLM Chemicals)},
      cin          = {W015},
      ddc          = {610},
      cid          = {I:(DE-He78)W015-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40608687},
      pmc          = {pmc:PMC12225867},
      doi          = {10.1371/journal.pone.0326373},
      url          = {https://inrepo02.dkfz.de/record/303062},
}