Frontiers in Cell and Developmental Biology (Jan 2022)

Rubicon in Metabolic Diseases and Ageing

  • Satoshi Minami,
  • Shuhei Nakamura,
  • Shuhei Nakamura,
  • Shuhei Nakamura,
  • Tamotsu Yoshimori,
  • Tamotsu Yoshimori,
  • Tamotsu Yoshimori

DOI
https://doi.org/10.3389/fcell.2021.816829
Journal volume & issue
Vol. 9

Abstract

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Autophagy is a conserved cellular degradation system that maintains intracellular homeostasis. Cytoplasmic components are engulfed into double-membrane vesicles called autophagosomes, which fuse with lysosomes, and resulting in the degradation of sequestered materials. Recently, a close association between autophagy and the pathogenesis of metabolic diseases and ageing has become apparent: autophagy is dysregulated during metabolic diseases and ageing; dysregulation of autophagy is intimately associated with the pathophysiology. Rubicon (Run domain Beclin-1 interacting and cysteine-rich containing protein) has been identified as a Beclin-1 associated protein. Notably, Rubicon is one of few negative regulators of autophagy whereas many autophagy-related genes are positive regulators of autophagy. Rubicon also has autophagy-independent functions including phagocytosis and endocytosis. In this mini-review, we focus on the various roles of Rubicon in different organs in the settings of metabolic diseases and ageing, and discuss its potential role as a promising therapeutic target.

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