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Autophagy01:27

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Autophagy is a self-digesting process by which a cell protects itself from threats both within and outside the cell, ranging from abnormal proteins to invading bacteria. In this process, obsolete components of the cell and invading microbes are degraded by hydrolytic enzymes active in an acidic environment of the lysosomal lumen.
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Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
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Cells undergoing apoptosis form apoptotic bodies that must be removed immediately to prevent inflammation, autoimmune diseases, and necrosis. Phagocytosis is carried out by professional phagocytes such as macrophages or  immature dendritic cells. Non-professional phagocytes such as  epithelial cells and fibroblasts also take part in this process; however, they are not as effective as professional phagocytes. 
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In Situ Immunofluorescent Staining of Autophagy in Muscle Stem Cells
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Coming back: autophagy in cachexia.

Fabio Penna1, Francesco M Baccino, Paola Costelli

  • 1Unit of Experimental and Clinical Pathology, Department of Clinical and Biological Sciences, University of Turin, Turin, Italy.

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Summary

Autophagy, a cellular process, plays a crucial role in muscle wasting during cachexia. Both excessive and deficient autophagy contribute to muscle loss, suggesting therapeutic potential.

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Area of Science:

  • Cellular Biology
  • Physiology
  • Pathology

Background:

  • Cachexia is a complex syndrome marked by weight loss, inflammation, and metabolic dysfunction.
  • Muscle wasting, a key feature of cachexia, results from increased protein degradation.
  • Autophagy's role in muscle wasting has been historically underestimated.

Purpose of the Study:

  • To review the involvement of autophagy in the pathogenesis of muscle wasting in cachexia.
  • To discuss the dual role of autophagy (excess and deficiency) in muscle depletion.
  • To explore potential therapeutic strategies targeting autophagy for muscle trophism.

Main Methods:

  • Literature review focusing on autophagy and muscle wasting in cachexia.
  • Analysis of studies investigating protein synthesis and degradation pathways.
  • Examination of evidence linking autophagy to various cachexia-inducing conditions.

Main Results:

  • Muscle mass regulation involves an imbalance between protein synthesis and degradation.
  • Autophagy-lysosome pathways, alongside ubiquitin-proteasome, contribute to muscle protein breakdown in cachexia.
  • Autophagy is implicated in muscle wasting associated with sepsis, COPD, cancer, and aging.

Conclusions:

  • Both excessive and defective autophagy are implicated in the development of muscle depletion.
  • Modulating autophagy presents a potential therapeutic avenue to improve muscle mass in cachexia.