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<p>Prolonged use of dexamethasone (DEX) increases intraocular pressure (IOP) and the risk of glaucoma. Recent studies have shown that DEX upregulates thrombospondin-1 (<i>THBS1</i>) gene expression and induces dysregulation of macroautophagy/autophagy in primary human trabecular meshwork (hTM) cells. Trehalose, a natural disaccharide, activates autophagy and protects cells against environmental stresses. Here, we report that trehalose-induced autophagy enhanced outflow facility, reduced IOP, and protected against ocular hypertension in mice. We analyzed autophagy induction by trehalose in hTM cells. Our data demonstrated that trehalose transcriptionally upregulated prototypical autophagy related genes and activated autophagy through the downregulation of <i>THBS1</i>. Consistent with prior findings, the results indicated that <i>THBS1</i> silencing or inhibition is a key cellular event for the regulation of aqueous humor outflow and IOP homeostasis. In conclusion, this study identified trehalose-induced autophagy as a protective mechanism against ocular hypertension which may have therapeutic potential.</p>

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The role of thrombospondin-1 in trehalose-induced autophagy and ocular hypertension in mice

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月6日

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  • Choi-ying Ling,
  • Kit-ying Choy,
  • Hoi-lam Li,
  • Choi-yee Tse,
  • Wei-ying Yang,
  • Nga-wai Wong,
  • W. Daniel Stamer,
  • Chi-wai Do,
  • Dennis Yan-yin Tse,
  • Samantha Sze-wan Shan

摘要

Prolonged use of dexamethasone (DEX) increases intraocular pressure (IOP) and the risk of glaucoma. Recent studies have shown that DEX upregulates thrombospondin-1 (THBS1) gene expression and induces dysregulation of macroautophagy/autophagy in primary human trabecular meshwork (hTM) cells. Trehalose, a natural disaccharide, activates autophagy and protects cells against environmental stresses. Here, we report that trehalose-induced autophagy enhanced outflow facility, reduced IOP, and protected against ocular hypertension in mice. We analyzed autophagy induction by trehalose in hTM cells. Our data demonstrated that trehalose transcriptionally upregulated prototypical autophagy related genes and activated autophagy through the downregulation of THBS1. Consistent with prior findings, the results indicated that THBS1 silencing or inhibition is a key cellular event for the regulation of aqueous humor outflow and IOP homeostasis. In conclusion, this study identified trehalose-induced autophagy as a protective mechanism against ocular hypertension which may have therapeutic potential.