pexophagy

Definition

Target type: biologicalprocess

The selective autophagy process in which a peroxisome is degraded by macroautophagy. [GOC:autophagy, PMID:12914914, PMID:16973210]

Pexophagy is a highly specialized form of autophagy that specifically targets peroxisomes for degradation. Peroxisomes are single-membrane-bound organelles found in almost all eukaryotic cells, playing crucial roles in various metabolic processes, including fatty acid β-oxidation, reactive oxygen species (ROS) detoxification, and biosynthesis of plasmalogens. Unlike general autophagy, which sequesters bulk cytoplasm, pexophagy exhibits a selective nature, ensuring the precise degradation of peroxisomes while preserving other cellular components. This specificity is achieved through intricate signaling pathways and a dedicated set of proteins that recognize and target peroxisomes for autophagic engulfment.

The process of pexophagy begins with the formation of a double-membrane structure known as the phagophore. This membrane originates from the endoplasmic reticulum (ER) and expands to envelop the targeted peroxisome. As the phagophore encloses the peroxisome, it forms a double-membrane vesicle called the autophagosome. The autophagosome then fuses with a lysosome, a cellular organelle containing hydrolytic enzymes. Inside the lysosome, the peroxisome is broken down into its constituent components, including proteins, lipids, and nucleic acids, which are recycled back into the cell.

Pexophagy is tightly regulated and can be triggered by various stimuli, including changes in nutrient availability, oxidative stress, and developmental cues. For instance, during periods of starvation, cells may degrade peroxisomes to provide energy and building blocks for survival. Conversely, pexophagy can also be induced by an increase in ROS production within peroxisomes, which can be detrimental to the cell. This selective removal of damaged peroxisomes ensures the maintenance of cellular homeostasis and prevents the accumulation of harmful ROS.

The molecular mechanisms underlying pexophagy are complex and involve a coordinated interplay of several key proteins. One crucial player is Atg8, a ubiquitin-like protein that conjugates to the phagophore membrane and acts as a receptor for cargo recognition. In pexophagy, Atg8 interacts with specific peroxisome-associated proteins, such as Pex3 and Pex14, facilitating the selective engulfment of peroxisomes. Other proteins involved in pexophagy include the autophagy-related proteins Atg5, Atg7, and Atg12, which are essential for phagophore elongation and closure.

The importance of pexophagy is highlighted by its involvement in various physiological processes and diseases. For instance, defects in pexophagy can lead to the accumulation of peroxisomes, resulting in various disorders, including Zellweger syndrome and neonatal adrenoleukodystrophy. These disorders are characterized by severe neurological and developmental impairments, demonstrating the crucial role of pexophagy in maintaining cellular function and health.

In conclusion, pexophagy is a fundamental cellular process that ensures the selective degradation and recycling of peroxisomes. This intricate mechanism involves specific signaling pathways, specialized proteins, and a coordinated series of events, ultimately contributing to cellular homeostasis and overall organismal health. Understanding the molecular basis of pexophagy provides insights into the regulation of organelle turnover, the pathogenesis of related diseases, and the potential therapeutic targets for these disorders.'
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Proteins (1)

Compounds (20)