Nature Communications (Mar 2023)

Enhanced Ca2+-channeling complex formation at the ER-mitochondria interface underlies the pathogenesis of alcohol-associated liver disease

  • Themis Thoudam,
  • Dipanjan Chanda,
  • Jung Yi Lee,
  • Min-Kyo Jung,
  • Ibotombi Singh Sinam,
  • Byung-Gyu Kim,
  • Bo-Yoon Park,
  • Woong Hee Kwon,
  • Hyo-Jeong Kim,
  • Myeongjin Kim,
  • Chae Won Lim,
  • Hoyul Lee,
  • Yang Hoon Huh,
  • Caroline A. Miller,
  • Romil Saxena,
  • Nicholas J. Skill,
  • Nazmul Huda,
  • Praveen Kusumanchi,
  • Jing Ma,
  • Zhihong Yang,
  • Min-Ji Kim,
  • Ji Young Mun,
  • Robert A. Harris,
  • Jae-Han Jeon,
  • Suthat Liangpunsakul,
  • In-Kyu Lee

DOI
https://doi.org/10.1038/s41467-023-37214-4
Journal volume & issue
Vol. 14, no. 1
pp. 1 – 18

Abstract

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Ca2+ overload-induced mitochondrial dysfunction is considered a contributing factor alcohol-associated liver disease pathogenesis. Here the authors report that PDK4 promotes Ca2 + -channelling complex formation at the endoplasmic reticulum-mitochondria contact sites, which contributes to the pathogenesis of alcohol-associated liver disease in studies with male mouse and hepatocyte models.