Department of Ophthalmology, Jinshan Hospital, Fudan University, Shanghai, China.
Department of Ophthalmology, Jinshan Hospital, Fudan University, Shanghai, China; Department of Central Laboratory, Jinshan Hospital, Fudan University, Shanghai, China.
Biochim Biophys Acta Mol Basis Dis. 2024 Mar;1870(3):166981. doi: 10.1016/j.bbadis.2023.166981. Epub 2023 Dec 14.
The role of extracellular matrix (ECM) remodeling in the axial elongation associated with myopia has not been fully elucidated, although it is considered a significant factor. EFEMP1, a regulator of ECM, has been associated with various pathological conditions. This study aimed to examine the involvement of EFEMP1 in scleral remodeling during form deprivation myopia. The results indicate a progressive increase in EFEMP1 expression following prolonged form deprivation treatment, followed by a subsequent decrease upon recovery. To gain a deeper understanding of the mechanism of EFEMP1, we conducted transcriptome sequencing on primary scleral fibroblasts that were subjected to lentivirus-mediated overexpression of EFEMP1. Validation was performed using lentivirus-induced overexpression and shRNA targeting EFEMP1 in combination with LY294002, a PI3K inhibitor. Our findings suggest that EFEMP1 may be involved in the development of FDM by regulating the expression of the PI3K/AKT/MMP2 axis. The AAV-mediated injection of shEFEMP1 under Tenon's capsule in guinea pigs was observed to effectively delay the progression of myopia and posterior scleral remodeling. In contrast, the AAV-mediated overexpression of EFEMP1 exacerbated the development of myopia and resulted in further thinning of collagen fibers in the posterior sclera. In summary, adjusting EFEMP1 concentrations could potentially serve as a viable approach to prevent and treat myopia by influencing the remodeling process of the posterior sclera.
细胞外基质(ECM)重塑在近视相关的轴向伸长中的作用尚未完全阐明,尽管它被认为是一个重要因素。EFEMP1 是 ECM 的调节剂,与各种病理状况有关。本研究旨在研究 EFEMP1 在形觉剥夺性近视(form deprivation myopia,FDM)中巩膜重塑中的作用。结果表明,在形觉剥夺治疗后,EFEMP1 的表达逐渐增加,随后在恢复后下降。为了更深入地了解 EFEMP1 的作用机制,我们对接受慢病毒介导的 EFEMP1 过表达的原代巩膜成纤维细胞进行了转录组测序。通过慢病毒诱导的 EFEMP1 过表达和 shRNA 靶向 EFEMP1 与 PI3K 抑制剂 LY294002 联合使用进行了验证。我们的研究结果表明,EFEMP1 可能通过调节 PI3K/AKT/MMP2 轴的表达参与 FDM 的发展。我们观察到,在豚鼠 Tenon 囊下用 AAV 介导的 shEFEMP1 注射可有效延缓近视和后巩膜重塑的进展。相反,AAV 介导的 EFEMP1 过表达加剧了近视的发展,并导致后巩膜胶原纤维进一步变薄。综上所述,通过影响后巩膜的重塑过程,调节 EFEMP1 的浓度可能是预防和治疗近视的一种可行方法。