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.
Highlights
Rubicon in Metabolic Diseases and AgeingCell Death and Survival, a section of the journal Frontiers in Cell and Developmental
The prevalence of metabolic diseases and age-related diseases is significantly increasing in the world (Christensen et al, 2009; Mozumdar and Liguori, 2011; von Ruesten et al, 2011; Ranasinghe et al, 2017; Foreman et al, 2018)
Accumulating evidence over the past decade indicates that autophagy has a key role in life span regulation (Hansen et al, 2018; Leidal et al, 2018; Nakamura and Yoshimori, 2018; Wong et al, 2020; Kaushik et al, 2021): autophagy is activated and required for the lifespan extension in various longevity paradigms, whereas autophagic activity is disturbed during the ageing process
Summary
Cell Death and Survival, a section of the journal Frontiers in Cell and Developmental. 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. 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 is one of few negative regulators of autophagy whereas many autophagy-related genes are positive regulators of autophagy. Rubicon has autophagy-independent functions including phagocytosis and endocytosis. In this minireview, 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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