Rubicon in Metabolic Diseases and Ageing

Satoshi Minami; Shuhei Nakamura; Tamotsu Yoshimori

doi:10.3389/fcell.2021.816829

Rubicon in Metabolic Diseases and Ageing

Front Cell Dev Biol. 2022 Jan 10:9:816829. doi: 10.3389/fcell.2021.816829. eCollection 2021.

Authors

Satoshi Minami¹, Shuhei Nakamura^{1

2

3}, Tamotsu Yoshimori^{1

2

4}

Affiliations

¹ Department of Genetics, Graduate School of Medicine, Osaka University, Suita, Japan.
² Department of Intracellular Membrane Dynamics, Graduate School of Frontier Biosciences, Osaka University, Suita, Japan.
³ Institute for Advanced Co-Creation Studies, Osaka University, Suita, Japan.
⁴ Integrated Frontier Research for Medical Science Division, Institute for Open and Transdisciplinary Research Initiatives, Osaka University, Suita, Japan.

Abstract

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.

Keywords: LAP; Rubicon; ageing; autophagy; longevity; metabolic disease.

Publication types

Review