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Related Concept Videos

Mitochondrial Membranes01:45

Mitochondrial Membranes

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A single mitochondrion is a bean-shaped organelle enclosed by a double-membrane system. The outer membrane of mitochondria is smooth and contains many porins - the integral membrane transporters. Porins enable free diffusion of ions and small uncharged molecules through the outer mitochondrial membrane but limit the transport of molecules larger than 5000 Daltons. Further, the outer mitochondrial membrane forms a unique structure called membrane contact sites with other subcellular organelles,...
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Mitochondrial Precursor Proteins01:39

Mitochondrial Precursor Proteins

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Mitochondrial precursors are partially unfolded or loosely folded polypeptide chains. Newly synthesized precursors are inhibited from spontaneously folding into their native conformation by the cytosolic chaperones, heat shock proteins 70 (Hsp70), and mitochondrial import stimulation factors (MSFs). Precursors bound to MSFs are guided to the TOM70-TOM37 receptors, while precursors bound to Hsp70  chaperones are targetted to TOM20-TOM22 receptor complexes.
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Animal Mitochondrial Genetics02:59

Animal Mitochondrial Genetics

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Among all the organelles in an animal cell, only mitochondria have their own independent genomes. Animal mitochondrial DNA is a double-stranded, closed-circular molecule with around 20,000 base pairs. Mitochondrial DNA is unique in that one of its two strands, the heavy, or H, -strand is guanine rich, whereas the complementary strand is cytosine rich and called the light, or L, -strand. Compared to nuclear DNA, mitochondrial DNA has a very low percentage of non-coding regions and is marked by...
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ATP Synthase: Mechanism01:48

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In animals, the mitochondrial F1F0 ATP synthase is the key protein that synthesizes ATP molecules through a complex catalytic mechanism. While the nuclear genome encodes the majority of ATP synthase subunits, the mitochondrial genome encodes some of the enzyme's most critical components. The formation of this multi-subunit enzyme is a complex multi-step process regulated at the level of transcription, translation, and assembly. Defects in one or more of these steps can result in decreased...
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Translocation of Proteins into the Mitochondria01:19

Translocation of Proteins into the Mitochondria

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Mitochondrial precursors are translocated to the internal subcompartments via independent mechanisms involving distinct protein machineries called translocases.
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Teratogenicity01:07

Teratogenicity

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The ability of a drug to produce structural deformations and functional abnormalities in the developing embryo or the fetus is called teratogenicity, and the drug producing this effect is known as a teratogen. Teratogenic effects include stillbirth, miscarriage, intrauterine growth restriction, and neurocognitive delay. A teratogen may affect the embryo at different stages of development, which is important in determining the type and extent of the damage. During blastocyst formation, the early...
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Updated: Aug 9, 2025

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

Published on: January 26, 2024

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Placental Mitochondrial Function and Dysfunction in Preeclampsia.

Fahmida Jahan1, Goutham Vasam2, Alex E Green1,2,3

  • 1Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, ON K1H 8M5, Canada.

International Journal of Molecular Sciences
|February 25, 2023
PubMed
Summary
This summary is machine-generated.

Mitochondrial dysfunction in the placenta is a key factor in preeclampsia (PE), a pregnancy disorder. Targeting placental mitochondria may offer new therapeutic strategies for PE subtypes.

Keywords:
disease subclasseshypertensionmitochondriaplacentapreeclampsiapregnancyreactive oxygen speciestherapies

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Area of Science:

  • Obstetrics and Gynecology
  • Maternal-Fetal Medicine
  • Mitochondrial Biology

Background:

  • The placenta is crucial for pregnancy, regulating nutrient exchange and fetal development.
  • Placental dysfunction can lead to adverse pregnancy outcomes, including preeclampsia (PE).
  • Preeclampsia is a heterogeneous hypertensive disorder with diverse clinical presentations, suggesting varied underlying placental pathologies.

Purpose of the Study:

  • To review evidence linking placental mitochondrial dysfunction to preeclampsia.
  • To explore how altered mitochondrial function may be a common factor across different PE subtypes.
  • To discuss advancements in targeting mitochondria for potential PE interventions.

Main Methods:

  • Review of existing scientific literature on placental pathology in preeclampsia.
  • Analysis of studies investigating mitochondrial function in PE placentas.
  • Synthesis of current research on therapeutic strategies targeting mitochondria.

Main Results:

  • Placental mitochondrial dysfunction is implicated in the pathogenesis of preeclampsia.
  • Altered mitochondrial function appears to be a shared feature across various forms of PE.
  • Evidence suggests distinct placental pathologies contribute to the heterogeneity of PE.

Conclusions:

  • Placental mitochondrial dysfunction is a significant contributor to preeclampsia development.
  • Targeting placental mitochondria presents a promising avenue for novel PE therapies.
  • Understanding mitochondrial roles may lead to subtype-specific treatments for preeclampsia.