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Related Concept Videos

Autophagy01:27

Autophagy

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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.
An autophagic pathway consists of a series of signaling events activated in response to diverse stress and physiological conditions such as food deprivation,...
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Delivery Pathways to the Lysosome01:36

Delivery Pathways to the Lysosome

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Eukaryotic cells use different mechanisms to eliminate toxic waste obsolete and worn-out substances. Lysosomes play a pivotal role in this, and hence, these substances are carried to the lysosome from other parts of the cell and extracellular space through different pathways. The most elaborately studied pathways to the lysosome are the endocytic pathways.
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In endocytosis, the cell membrane takes up macromolecules and particles from the surrounding medium. Clathrin-mediated...
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Autophagic Cell Death01:18

Autophagic Cell Death

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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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Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and...
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The Proteasome01:13

The Proteasome

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Eukaryotic cells can degrade proteins through several pathways. One of the most important among these is the ubiquitin-proteasome pathway. It helps the cell eliminate the misfolded, damaged, or unwarranted cytoplasmic proteins in a highly specific manner.
In this pathway, the target proteins are first tagged with small proteins called ubiquitin. This involves participation of a series of enzymes including— E1 (ubiquitin-activating enzyme), E2 (ubiquitin-conjugating enzyme), and E3...
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Phagocytosis of Apoptotic Cells01:17

Phagocytosis of Apoptotic Cells

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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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Apoptosis01:30

Apoptosis

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Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size...
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Updated: Jun 4, 2025

Activating Autophagy by Aerobic Exercise in Mice
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Activating Autophagy by Aerobic Exercise in Mice

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Exercise-driven cellular autophagy: A bridge to systematic wellness.

Xiao-Han Zhou1, Ya-Xi Luo1, Xiu-Qing Yao2

  • 1Department of Rehabilitation, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, PR China.

Journal of Advanced Research
|January 5, 2025
PubMed
Summary
This summary is machine-generated.

Exercise activates autophagy, a cellular process vital for health. Understanding how different exercise types influence autophagy is key to harnessing its benefits for disease prevention and longevity.

Keywords:
AutophagyExerciseHealthMacroautophagyPhysical activityWell-being

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Area of Science:

  • Cellular Biology
  • Exercise Physiology
  • Molecular Mechanisms

Background:

  • Exercise promotes health by maintaining homeostasis and aiding recovery.
  • Autophagy, a cellular process, is crucial for balance, but its dysregulation contributes to disease.
  • The interplay between exercise and autophagy is not fully understood.

Purpose of the Study:

  • To explore molecular mechanisms of exercise-induced autophagy across tissues.
  • To examine how exercise modality influences autophagic responses and cellular balance.
  • To highlight signaling pathways involved in organ protection, disease risk reduction, and longevity.

Main Methods:

  • Review of molecular mechanisms linking exercise to autophagy.
  • Analysis of signaling pathways (AMPK, mTOR, PI3K/Akt) in response to exercise.
  • Examination of exercise's impact on cellular homeostasis and proteostasis.

Main Results:

  • Exercise-induced autophagy is modulated by exercise type, intensity, duration, and individual factors.
  • Aerobic exercise activates AMPK/mTOR; anaerobic training activates PI3K/Akt.
  • Exercise-induced autophagy benefits conditions like sarcopenia, neurodegeneration, and metabolic disorders.
  • Excessive exercise can lead to detrimental autophagic overactivation.

Conclusions:

  • Exercise-induced autophagy is a dynamic process crucial for cellular and systemic health.
  • Balanced exercise regimens are essential to maximize therapeutic benefits and minimize risks.
  • Future research should focus on biomarkers, optimized protocols, and combined strategies.