Macroautophagy, commonly referred to as autophagy, is a self-degradation process through which virtually all eukaryotic cells sequester cytoplasmic components (macromolecules, but also entire organelles or microorganisms) into de novo formed, double-membrane vescicles (autophagosomes) and degrade them after lysosomal fusion. The degradation products released from lysosomes are recycled into metabolic and biosynthetic pathways. Autophagy, normally occurring for ordinary organelle and protein turnover, can be enhanced in stress conditions as an adaptive, survival response to microenvironmental and intracellular noxia, including glucose, amino acid or growth factors withdrawal, hypoxia, oxidative stress, mitochondrial or organelle dysfunction, infections, and cytotoxic drugs. However, an excessive or long-lasting activation of autophagy can culminate in a peculiar mode of cell death. An imbalanced autophagy (either unrestrained or deficient) plays a role in the pathogenesis of different diseases, including cancer, neurodegenerative diseases, cardiovascular and autoimmune pathologies. In tumor cells, however, autophagy proves to play an ambiguous dual role (protective or cytotoxic), possibly depending on tumor cell type, genetic background and tumor stage.

Maellaro, E. (2018). Autophagy: a self-eating process in cell physiology and pathology [Autofagia: un processo fisiopatologico di autodigestione cellulare]. LA RIVISTA ITALIANA DELLA MEDICINA DI LABORATORIO, 14(3), 136-140 [10.1007/s13631-018-0194-x].

Autophagy: a self-eating process in cell physiology and pathology [Autofagia: un processo fisiopatologico di autodigestione cellulare]

Maellaro, Emilia
2018-01-01

Abstract

Macroautophagy, commonly referred to as autophagy, is a self-degradation process through which virtually all eukaryotic cells sequester cytoplasmic components (macromolecules, but also entire organelles or microorganisms) into de novo formed, double-membrane vescicles (autophagosomes) and degrade them after lysosomal fusion. The degradation products released from lysosomes are recycled into metabolic and biosynthetic pathways. Autophagy, normally occurring for ordinary organelle and protein turnover, can be enhanced in stress conditions as an adaptive, survival response to microenvironmental and intracellular noxia, including glucose, amino acid or growth factors withdrawal, hypoxia, oxidative stress, mitochondrial or organelle dysfunction, infections, and cytotoxic drugs. However, an excessive or long-lasting activation of autophagy can culminate in a peculiar mode of cell death. An imbalanced autophagy (either unrestrained or deficient) plays a role in the pathogenesis of different diseases, including cancer, neurodegenerative diseases, cardiovascular and autoimmune pathologies. In tumor cells, however, autophagy proves to play an ambiguous dual role (protective or cytotoxic), possibly depending on tumor cell type, genetic background and tumor stage.
Maellaro, E. (2018). Autophagy: a self-eating process in cell physiology and pathology [Autofagia: un processo fisiopatologico di autodigestione cellulare]. LA RIVISTA ITALIANA DELLA MEDICINA DI LABORATORIO, 14(3), 136-140 [10.1007/s13631-018-0194-x].
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11365/1070414