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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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Lysosomes are the site for the degradation of macromolecules and biological polymers released during membrane trafficking events such as secretory, endocytic, autophagic, and phagocytic pathways. The membrane-enclosed area of the lysosome, called the lumen, contains hydrolytic enzymes active in an acidic environment. These acid hydrolases are functional at a pH between 4.5 and 5 and are involved in cellular processes such as cell signaling, energy metabolism, restoration of the plasma membrane,...
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Related Experiment Video

Updated: Mar 29, 2026

Author Spotlight: Modeling an Aspect of Preeclampsia in Female Mice Using Hypoxic Human Placenta-Derived Small Extracellular Vesicles
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Author Spotlight: Modeling an Aspect of Preeclampsia in Female Mice Using Hypoxic Human Placenta-Derived Small Extracellular Vesicles

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Revised Two-Stage Model of Preeclampsia Based on Autophagic Dysfunction: A Comprehensive Review.

Atsushi Furuta1, Tomoko Shima1, Takashi Nishigori1

  • 1Department of Obstetrics and Gynecology, University of Toyama, Toyama 930-0194, Japan.

Biomolecules
|March 28, 2026
PubMed
Summary
This summary is machine-generated.

Preeclampsia may stem from impaired autophagy, a cellular process crucial for early placental development. This study proposes a new model linking autophagy dysfunction to placental issues and maternal syndrome.

Keywords:
TFEBautophagypreeclampsia

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Area of Science:

  • Obstetrics and Gynecology
  • Cellular Biology
  • Pathophysiology

Background:

  • Preeclampsia pathogenesis remains incompletely understood.
  • Early placentation involves extravillous trophoblast invasion into the myometrium under challenging conditions.
  • The 'One-Third Myometrium Enigma' highlights the necessity of trophoblast traversal to this region.

Purpose of the Study:

  • To propose a revised two-stage model of preeclampsia.
  • To investigate the role of autophagy in extravillous trophoblast invasion.
  • To link autophagic dysfunction to preeclampsia development and maternal syndrome.

Main Methods:

  • Proposed a two-stage model centered on autophagy.
  • Hypothesized timed rise in basal autophagy and TFEB-driven lysosomal programs.
  • Identified potential failure modes including impaired autophagic flux and persistent hypoxia signaling.

Main Results:

  • Autophagic dysfunction may lead to shallow trophoblast invasion, placental hypoxia, and fetal growth restriction.
  • Impaired autophagy is suggested as a contributor to preeclampsia.
  • Dysfunction can arise from inhibited autophagosome-lysosome fusion or prolonged HIF-1α activity.

Conclusions:

  • Preeclampsia can be reframed as a disorder of placental quality control.
  • Impaired autophagy is a testable contributor to preeclampsia pathogenesis.
  • Future directions include risk stratification using autophagy markers and therapeutic modulation of autophagy.