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Glucose-mediated mitochondrial reprogramming by cholesterol export at TM4SF5-enriched mitochondria-lysosome contact sites.

Ji Eon KimSo-Young ParkChulhwan KwakYoonji LeeDae-Geun SongJae Woo JungHaesong LeeEun-Ae ShinYangie PinangaKyung-Hee PyoEun Hae LeeWonsik KimSoyeon KimChang-Duck JunJeanho YunSun ChoiHyun-Woo RheeKwang-Hyeon LiuJung Weon Lee
Published in: Cancer communications (London, England) (2023)
Our findings suggested that TM4SF5-enriched MLCSs regulate glucose catabolism by facilitating cholesterol export for mitochondrial reprogramming, presumably while hepatocellular carcinogenesis, recapitulating aspects for hepatocellular carcinoma metabolism with mitochondrial reprogramming to support biomolecule synthesis in addition to glycolytic energetics.
Keyphrases
  • oxidative stress
  • blood glucose
  • low density lipoprotein
  • cell death
  • type diabetes
  • metabolic syndrome
  • blood pressure
  • skeletal muscle
  • living cells
  • weight loss