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Updated: Oct 27, 2025

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SLC39A5 dysfunction impairs extracellular matrix synthesis in high myopia pathogenesis.

Shanshan Dong1, Qi Tian1, Tengfei Zhu2

  • 1Center for Medical Genetics & Hunan Key Laboratory of Medical Genetics, School of Life Sciences, Central South University, Changsha, Hunan, China.

Journal of Cellular and Molecular Medicine
|July 24, 2021
PubMed
Summary

SLC39A5 depletion causes zinc deficiency, destabilizing Smad proteins and inhibiting TGF-β signaling. This impairs extracellular matrix synthesis, contributing to high myopia pathogenesis.

Keywords:
ECMSLC39A5SmadTGF-β signallinghigh myopiazinc

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Area of Science:

  • Genetics
  • Molecular Biology
  • Ophthalmology

Background:

  • High myopia is a leading cause of visual impairment with high heritability.
  • Previous studies identified SLC39A5's genetic role in high myopia and its regulation of the TGF-β pathway.

Purpose of the Study:

  • To elucidate the mechanisms of SLC39A5 in high myopia pathogenesis.
  • To investigate the link between SLC39A5, zinc transport, and TGF-β signaling in myopia development.

Main Methods:

  • Utilized SLC39A5 knockout (KO) human embryonic kidney cells (HEK293).
  • Performed RNA-sequencing (RNA-seq) and quantitative reverse transcription PCR (qRT-PCR) to analyze gene expression.
  • Assessed cell morphogenesis, migration, and extracellular matrix (ECM) constituent integrity.
  • Investigated TGF-β signaling pathway activation, Smad protein stability, and intracellular zinc levels.

Main Results:

  • SLC39A5 KO cells exhibited abnormal morphogenesis, migration, and ECM injury.
  • Decreased transcription of key ECM genes (COL1A1, COL2A1, COL4A1, FN1, LAMA1) was observed in KO cells.
  • TGF-β signaling was inhibited in SLC39A5-depleted cells, with blocked R-Smad phosphorylation.
  • Intracellular zinc deficiency due to SLC39A5 depletion destabilized Smad proteins, inhibiting TGF-β signaling and ECM synthesis.

Conclusions:

  • SLC39A5 depletion leads to zinc deficiency, which destabilizes Smad proteins.
  • This destabilization inhibits TGF-β signaling and downstream ECM synthesis, contributing to high myopia.
  • Findings offer insights into the molecular mechanisms underlying myopic development.