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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.
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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.
Endocytosis
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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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Autocrine Signaling01:01

Autocrine Signaling

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Autocrine signaling is one of the many signaling mechanisms that function inside multicellular organisms to carry out intercellular communication. In this type of signaling mechanism, the same cell that secretes an extracellular signaling molecule also expresses the receptors to bind and respond to that signaling molecule.
Autocrine Signaling in Macrophages
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The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

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Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
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mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

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The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
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Updated: Jun 27, 2025

Exploring the Regulation of Lipid Droplet Catabolism through Lipophagy
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Exploring the Regulation of Lipid Droplet Catabolism through Lipophagy

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The link between autophagy and psoriasis.

Nannan Liang1, Kaiming Zhang1

  • 1Shanxi Key Laboratory of Stem Cell for Immunological Dermatosis, Institute of Dermatology, Taiyuan Central Hospital of Shanxi Medical University, Taiyuan, Shanxi, China.

Acta Histochemica
|April 30, 2024
PubMed
Summary
This summary is machine-generated.

Autophagy, a cellular renewal process, is crucial for skin health. Reduced autophagy contributes to psoriasis, suggesting that enhancing this mechanism could be a novel therapeutic strategy for managing psoriasis.

Keywords:
AutophagyKeratinocyteMesenchymal stem cellPsoriasisT cell

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Area of Science:

  • Cell Biology
  • Immunodermatology
  • Molecular Medicine

Background:

  • Autophagy is a fundamental cellular process for degrading and recycling cellular components, essential for maintaining intracellular homeostasis.
  • Psoriasis is a chronic inflammatory skin disease characterized by epidermal hyperproliferation, immune cell infiltration, and altered differentiation.
  • Autophagy plays significant roles in various skin-resident cells, including keratinocytes and mesenchymal stem cells (MSCs).

Purpose of the Study:

  • To review the role of autophagy in the pathogenesis of psoriasis.
  • To explore therapeutic strategies targeting autophagy modulation for psoriasis treatment.

Main Methods:

  • Literature review of studies investigating autophagy in psoriasis.
  • Analysis of the functions of autophagy in cutaneous cells like keratinocytes, MSCs, T cells, and endothelial cells.

Main Results:

  • Autophagy regulates critical functions in skin cells relevant to psoriasis pathogenesis.
  • Evidence suggests that impaired autophagy contributes to the development and progression of psoriasis.
  • Modulating autophagy impacts inflammatory responses and cellular homeostasis in the skin.

Conclusions:

  • Autophagy is a key regulator of cutaneous cell function and homeostasis.
  • Reduced autophagy is implicated in psoriasis pathogenesis.
  • Enhancing autophagy presents a promising therapeutic avenue for mitigating psoriasis.