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Related Concept Videos

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.
Sorting of outer membrane proteins:
Mitochondrial outer membrane proteins are of two types: the transmembrane, beta-barrel porins, and the membrane-anchored, alpha-helical proteins. Beta-barrel porin precursors are translocated by the TOM complex and inserted into the outer mitochondrial membrane by the SAM complex. In contrast,...
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Glucose Transporters01:27

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Glucose transporters facilitate the transport of glucose across the cell membrane. In addition to glucose, some glucose transporters can also aid the movement of other hexoses such as fructose, mannose, and galactose.
Facilitated diffusion-glucose transporters (GLUTs) are encoded by the solute-linked carrier (SLC) family 2, subfamily A gene family, or SLC2A. The 14 GLUT protein members are distributed into three classes:
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Electron Transport Chain: Complex I and II01:46

Electron Transport Chain: Complex I and II

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The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
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Insulin Secretory Vesicles01:05

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Insulin secretory vesicles release insulin to stimulate blood glucose uptake and regulate carbohydrate metabolism. When the blood glucose levels increase, glucose enters the pancreatic β-islet cells through glucose transporters. Once inside, glucose is metabolized through glycolysis, the citric acid cycle, and the electron transport chain, producing ATP. This increase in ATP concentration closes ATP-sensitive potassium channels, leading to depolarization of the membrane and the opening of...
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Chemiosmosis01:32

Chemiosmosis

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Oxidative phosphorylation is a highly efficient process that generates large amounts of adenosine triphosphate (ATP), the basic unit of energy that drives many cellular processes. Oxidative phosphorylation involves two processes— the electron transport chain and chemiosmosis.
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Energy to Drive Translocation01:37

Energy to Drive Translocation

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Mitochondrial protein import is powered by two distinct energy sources: ATP hydrolysis and electrochemical potential across the inner membrane. Newly synthesized precursors are bound by cytosolic chaperones of the Hsp70 family, which guide them to the import receptors on the mitochondrial surface. Utilizing the energy of ATP hydrolysis, Hsp70 chaperones transfer these precursors to the TOM receptors on the mitochondrial outer membrane.
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Related Experiment Video

Updated: May 23, 2025

Visualization of Endogenous Mitophagy Complexes In Situ in Human Pancreatic Beta Cells Utilizing Proximity Ligation Assay
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Syntaxin 17 Translocation Mediated Mitophagy Switching Drives Hyperglycemia-Induced Vascular Injury.

Anqi Luo1, Rui Wang2, Jingwen Gong3

  • 1School of Pharmacy, China Pharmaceutical University, Nanjing, 211198, China.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|March 26, 2025
PubMed
Summary

Diabetic cardiovascular complications are worsened by prolonged high glucose, which switches mitophagy from Parkin-mediated to STX17-mediated pathways, causing endothelial injury. Targeting this mitophagy switch offers new therapeutic strategies.

Keywords:
(diabetesFis1Syntaxin 17)mitophagyvascular endothelial injury

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Area of Science:

  • Cardiovascular Science
  • Cell Biology
  • Metabolic Disorders

Background:

  • Diabetic cardiovascular complications correlate with hyperglycemia duration.
  • Mitophagy is implicated in vascular endothelial injury, but mechanisms remain unclear.
  • Understanding mitophagy's role in hyperglycemia-induced endothelial dysfunction is critical.

Purpose of the Study:

  • To elucidate the mechanisms of mitophagy in endothelial injury during sustained hyperglycemia.
  • To investigate the roles of Parkin, Fis1, and STX17 in high-glucose-induced mitophagy.
  • To identify potential therapeutic targets for diabetic cardiovascular complications.

Main Methods:

  • Utilized diabetic ApoE-/- mice and human umbilical vein endothelial cell (HUVEC) models.
  • Analyzed mitophagy pathways (Parkin-mediated and STX17-mediated) under short-term and long-term high-glucose conditions.
  • Investigated the effects of silencing or overexpressing STX17 and Fis1 on endothelial function, ROS levels, and eNOS phosphorylation.

Main Results:

  • Short-term high glucose enhanced Parkin-mediated mitophagy and upregulated Fis1.
  • Long-term high glucose suppressed Parkin-mediated mitophagy, downregulated Fis1, and activated STX17-mediated mitophagy.
  • STX17 silencing alleviated mitochondrial degradation and endothelial injury, while Fis1 silencing exacerbated it.

Conclusions:

  • The switch from Parkin-mediated to STX17-mediated mitophagy drives vascular endothelial injury in long-term hyperglycemia.
  • STX17 and Fis1 play critical, opposing roles in regulating mitophagy and endothelial function under hyperglycemic stress.
  • These findings provide insights for developing therapeutic strategies against diabetic cardiovascular complications.