Abstract

Autophagy is a conserved method of quality control in which cytoplasmic contents are degraded via lysosomes. Lipophagy, a form of selective autophagy and a novel type of lipid metabolism, has recently received much attention. Lipophagy is defined as the autophagic degradation of intracellular lipid droplets (LDs). Although much remains unknown, lipophagy appears to play a significant role in many organisms, cell types, metabolic states, and diseases. It participates in the regulation of intracellular lipid storage, intracellular free lipid levels (e.g., fatty acids), and energy balance. However, it remains unclear how intracellular lipids regulate autophagy. Impaired lipophagy can cause cells to become sensitive to death stimuli and may be responsible for the onset of a variety of diseases, including nonalcoholic fatty liver disease and metabolic syndrome. Like autophagy, the role of lipophagy in cancer is poorly understood, although analysis of specific autophagy receptors has helped to expand the diversity of chemotherapeutic targets. These studies have stimulated increasing interest in the role of lipophagy in the pathogenesis and treatment of cancer and other human diseases.

Highlights

  • Autophagy has been intensely studied since its discovery

  • Autophagy is divided into three subtypes (macroautophagy, chaperone-mediated autophagy (CMA), and microautophagy), which can be nonselective or selective [5] and include the selective removal of damaged mitochondria by mitophagy and the selective removal of endoplasmic reticulum components by phagocytosis [3, 5–7]

  • In view of the previously shown important role of lipid metabolism Lipophagy has been shown to play a role in various diseases; in liver homeostasis, impaired lipid metabolism may be an targeted stimulation of lipophagy represents a feasible method of important factor in excessive lipid accumulation and steatosis in treating fatty liver disease, while in nonalcoholic fatty liver disease (NAFLD), activation of the liver, which leads to serious consequences of alcoholic and autophagy/lipophagy is being studied [48, 49]

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Summary

Introduction

Autophagy has been intensely studied since its discovery. As one of the two evolutionarily conserved cell degradation pathways (autophagic degradation and proteasomal degradation), autophagy maintains a dynamic intracellular balance and can be activated by a variety of different stresses [1–4]. Knockout of LAL leads to accumulation of many small LDs in a p62 has been widely studied in a variety of signal transduction manner dependent on lipolysis driven by upstream ATGL, and pathways, many of which are related to cell survival and death inhibition of ATGL affects the shape and size of LDs more rapidly.

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