Conjunctival fibrosis is a process of extracellular matrix accumulation and the appearance of myofibroblasts in subconjunctival fibroblasts induced by injury or inflammation, which can significantly reduce the filtration efficiency of glaucoma filtration surgery. In this study, autophagy was confirmed to be involved in regulating the fibrosis of human subconjunctival fibroblasts (hSCFs) induced by TGF-β1. Following the addition of rapamycin, we detected that autophagy activation could reduce the increased expression level of αSMA and the accumulation of extracellular matrix component proteins namely fibronectin and type I collagen induced by TGF-β1 via the inhibition of SMAD2 phosphorylation. Following the addition of HCQ, the inhibition of autophagy aggravated TGF-β1-induced fibrosis of hSCFs. We further verified that trehalose, a safe clinical drug, could alleviate TGF-β1-induced fibrosis of hSCFs by activating autophagy and that these effects could be blocked by autophagy inhibition. In summary, autophagy was shown to be involved in the regulation of TGF-β1-induced fibrosis of hSCFs, which provided a novel perspective for exploring the progression of this lesion. More importantly, the protective effects of trehalose on TGF-β1-induced fibrosis of hSCFs were mediated by the activation of autophagy and could provide possible new approaches for the clinical treatment of conjunctival fibrosis.

中文翻译：

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海藻糖通过激活自噬减弱TGF-β1诱导的hSCF纤维化。

结膜纤维化是由损伤或炎症引起的结膜下亚成纤维细胞中细胞外基质积聚和肌成纤维细胞出现的过程，可显着降低青光眼滤过手术的滤过效率。在这项研究中，自噬被证实与调节由TGF-β1诱导的人结膜下成纤维细胞（hSCFs）的纤维化有关。加入雷帕霉素后，我们发现自噬激活可以通过抑制SMAD2磷酸化来降低αSMA的表达水平增加和TGF-β1诱导的细胞外基质成分蛋白纤连蛋白和I型胶原蛋白的积累。加入HCQ后，自噬的抑制加剧了TGF-β1诱导的hSCF纤维化。我们进一步验证了海藻糖，一种安全的临床药物，可以通过激活自噬减轻TGF-β1诱导的hSCF纤维化，并且这些作用可以被自噬抑制所阻断。总之，自噬被证明与TGF-β1诱导的hSCF纤维化的调节有关，这为探索该病变的进展提供了新的视角。更重要的是，海藻糖对TGF-β1诱导的hSCF纤维化的保护作用是通过自噬的激活介导的，可以为结膜纤维化的临床治疗提供可能的新途径。为探索该病变的进展提供了新颖的视角。更重要的是，海藻糖对TGF-β1诱导的hSCF纤维化的保护作用是通过自噬的激活介导的，可以为结膜纤维化的临床治疗提供可能的新途径。为探索该病灶的进展提供了新颖的视角。更重要的是，海藻糖对TGF-β1诱导的hSCF纤维化的保护作用是通过自噬的激活介导的，可以为结膜纤维化的临床治疗提供可能的新途径。