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Related Concept Videos

Delivery Pathways to the Lysosome01:36

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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.
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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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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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Autophagy01:27

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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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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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After folding, the ER assesses the quality of secretory and membrane proteins. The correctly folded proteins are cleared by the calnexin cycle for transport to their final destination, while misfolded proteins are held back in the ER lumen. The ER chaperones attempt to unfold and refold the misfolded proteins but sometimes fail to achieve the correct native conformation. Such terminally misfolded proteins are then exported to the cytosol by ER-associated degradation or ERAD pathway for...
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Related Experiment Video

Updated: Nov 11, 2025

Author Spotlight: Detection of Mitophagy in Caenorhabditis elegans and Mammalian Cells Using Organelle-Specific Dyes
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Deficient mitophagy pathways in sickle cell disease.

Suella Martino1,2,3, Jean-Benoit Arlet3,4, Marie-Hélène Odièvre1,2,3,5

  • 1Université de Paris, Inserm, Biologie Intégrée du Globule Rouge, Paris, France.

British Journal of Haematology
|March 23, 2021
PubMed
Summary

Sickle cell disease patients can have elevated mitochondria in red blood cells. This abnormal retention is linked to reduced mitophagy and impacts disease characteristics.

Keywords:
PINK1/NIXmitochondriamitophagysickle cell disease

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Area of Science:

  • Hematology
  • Cell Biology
  • Biochemistry

Background:

  • Sickle cell disease (SCD) involves chronic hemolysis and oxidative stress.
  • Red blood cells (RBCs) typically lack mitochondria in adults.

Purpose of the Study:

  • Investigate mitochondrial presence and function in RBCs of SCD patients.
  • Explore the role of mitophagy in mitochondrial retention in SCD.

Main Methods:

  • Analyzed 30 SCD patients' mature RBCs for mitochondria levels.
  • Assessed reticulocytosis, total bilirubin, and fetal hemoglobin.
  • Measured mitophagy inducers (PINK1, NIX) and HSP90 chaperone levels.

Main Results:

  • 40% of SCD patients (SS-mito+) showed elevated mitochondria in RBCs.
  • SS-mito+ group had higher reticulocytosis, bilirubin, lower fetal hemoglobin, and non-functional mitochondria.
  • Decreased mitophagy inducers (PINK1, NIX) and increased HSP90 were observed in SS-mito+ RBCs.

Conclusions:

  • Identified abnormal mitochondria retention in a subset of SCD patients.
  • Linked mitochondrial retention to impaired mitophagy pathways.
  • Suggests a novel mechanism contributing to SCD pathophysiology.