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Network Pharmacology and Validation of the Antidepressant Mechanisms of Qiangzhifang in a Chronic Restraint Stress-induced Depression Rat Model
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FKBP5/FKBP51 enhances autophagy to synergize with antidepressant action

Nils C Gassen1, Jakob Hartmann, Mathias V Schmidt

  • 1a Department of Translational Research in Psychiatry ; Max Planck Institute of Psychiatry ; Munich , Germany.

Autophagy
|February 26, 2015
PubMed

Insights

Antidepressants increase autophagy, a cellular process. Our findings show the cochaperone FKBP5 (FK506 binding protein 5) is essential for this effect and for antidepressant action in cells, mice, and humans.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Molecular Biology

Background:

  • Antidepressant treatment increases autophagy markers in cells.
  • The precise role of autophagy in antidepressant action and its connection to other pathways remained unclear.

Purpose of the Study:

  • To investigate the role of the cochaperone FKBP5 (FK506 binding protein 5) in mediating the autophagic effects of antidepressants.
  • To determine if FKBP5 is a prerequisite for antidepressant action.

Main Methods:

  • Studied the association of FKBP5 with BECN1.
  • Assessed changes in FKBP5 phosphorylation and protein levels.
  • Measured markers of autophagy and autophagic flux in cells, mice, and human samples.
  • Investigated the dependence of antidepressant effects on FKBP5.

Main Results:

  • FKBP5 associates with BECN1, altering its phosphorylation and protein levels.
  • FKBP5 enhances autophagy markers and autophagic flux.
  • The physiological effects of antidepressants in mice and humans are dependent on FKBP5.

Conclusions:

  • FKBP5 plays a crucial role in autophagy.
  • FKBP5 is a prerequisite for antidepressant action, influencing both cellular and physiological effects.
  • Targeting FKBP5 may offer new therapeutic strategies for depression.
Keywords:
Beclin 1FKBP5FKBP51antidepressantautophagydepression

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