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Related Concept Videos

Protein Import into the Peroxisomes01:27

Protein Import into the Peroxisomes

3.3K
Cells contain membrane-bound organelles called peroxisomes that oxidize organic molecules by transferring hydrogen atoms to oxygen, producing hydrogen peroxide. Peroxisomes enzymatically convert the released hydrogen peroxide into water and oxygen.
Peroxisomal Protein Import:
Peroxisomes lack the genetic machinery required to code for their own proteins. Hence, most peroxisomal membrane, lumenal and transmembrane proteins are synthesized in the cytoplasm or ER and transported to the peroxisome...
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Peroxisomes01:24

Peroxisomes

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Peroxisomes are specialized organelles present in fungi, plant, and animal cells. It can vary in number, size, morphology, and activity depending on the type of tissue and the nutritional state of the cell. For example, cells with active lipid metabolism, such as adipocytes, neurons, and hepatocytes, have more peroxisomes than other cells in the body. Besides their primary role in breaking down complex organic molecules, peroxisomes can also synthesize specific macromolecules and participate in...
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Genome-wide screen identifies peroxisomal role in APOL1 podocytopathy.

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Genomewide Screen Identifies Peroxisomal Role in APOL1 Podocytopathy.

Jiyoung Kim1, Isaac Z Karel1, Huijuan Song2

  • 1Division of Pharmaceutics and Pharmacology, College of Pharmacy and Comprehensive Cancer Center, The Ohio State University, Columbus, OH.

Medrxiv : the Preprint Server for Health Sciences
|March 4, 2025
PubMed
Summary
This summary is machine-generated.

The APOL1 gene variants linked to chronic kidney disease (CKD) are worsened by hypoxia. Peroxisome function is key, as enhancing it reduces cell death, suggesting a new therapeutic target for CKD.

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Area of Science:

  • Genetics
  • Cell Biology
  • Nephrology

Background:

  • The APOL1 gene G1 and G2 variants are risk factors for chronic kidney disease (CKD) in individuals of African descent.
  • Secondary stressors like hypoxia exacerbate APOL1 variant-induced podocyte dysfunction and cell death through incompletely understood mechanisms.

Purpose of the Study:

  • To identify genes influencing the cytotoxic effects of APOL1 variants under hypoxic conditions.
  • To elucidate the role of peroxisomes in APOL1-related kidney disease pathogenesis.

Main Methods:

  • Conducted a whole-genome RNA interference (RNAi) screen to identify genes modulating APOL1 variant cytotoxicity.
  • Utilized genetic and pharmacological approaches to enhance peroxisomal function.
  • Identified and mutated a peroxisomal targeting signal (PTS) in APOL1.

Main Results:

  • Silencing of several peroxisomal (PEX) genes significantly intensified APOL1 variant-induced cytotoxicity.
  • Enhanced peroxisomal function, genetically or pharmacologically, markedly reduced APOL1 variant cytotoxicity.
  • A C-terminal peroxisomal targeting signal (PTS) in APOL1 was identified; mutations in this signal attenuated variant cytotoxicity.

Conclusions:

  • Peroxisomal function plays a critical, previously unrecognized role in the pathogenesis of APOL1-associated CKD.
  • Targeting peroxisomes presents a potential therapeutic strategy to reduce CKD risk in populations carrying APOL1 risk variants.