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Counting and Determining the Viability of Cultured Cells
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Oh cystinosin: let me count the ways!

Craig B Langman1

  • 1Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA; The Ann and Robert H. Lurie Children's Hospital of Chicago, Chicago, Illinois, USA.

Kidney International
|July 24, 2019
PubMed
Summary

Nephropathic cystinosis, a genetic disorder, stems from faulty cystinosin protein. New research identifies galectin-3 as a key factor in the disease

Area of Science:

  • * Molecular biology and genetic disorders
  • * Lysosomal storage diseases

Background:

  • * Nephropathic cystinosis is the primary genetic cause of renal Fanconi syndrome.
  • * It results from the dysfunction of the lysosomal cystine-transporter protein, cystinosin.
  • * Previously, organ damage was attributed to defective protein and cystine crystals, though crystals were not consistently found.

Purpose of the Study:

  • * To explore additional cellular processes involved in nephropathic cystinosis pathogenesis.
  • * To investigate the role of galectin-3 in the disease.

Main Methods:

  • * Review of existing literature on cystinosis biology.
  • * Analysis of cellular mechanisms beyond cystine accumulation.

Main Results:

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  • * The study expands the understanding of cystinosis beyond cystine crystal formation.
  • * Galectin-3 is identified as a newly recognized pathogenic factor in nephropathic cystinosis.

Conclusions:

  • * Pathogenesis of nephropathic cystinosis involves multiple cellular processes.
  • * Galectin-3 represents a novel target for understanding and potentially treating the disease.