Department of Neurosurgery, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China.
Shaanxi Eye Hospital, Xi'an People's Hospital (Xi'an Fourth Hospital), Affiliated People's Hospital of Northwest University, Xi'an, Shaanxi, China.
Curr Eye Res. 2024 Nov;49(11):1193-1200. doi: 10.1080/02713683.2024.2363473. Epub 2024 Jun 10.
Ischemic retinopathy is the major cause of vision-threatening conditions. Inflammation plays an important role in the pathogenesis of ischemic retinopathy. Formyl peptide receptor 1 (FPR1) has been reported to be implicated in the regulation of inflammatory disorders. However, the role of FPR1 in the progression of ischemic retinal injury has not been fully explained.
The activation of FPR1 was measured by real-time PCR and western blotting in the retina of OIR. The effect of FPR1 on the expression of inflammatory cytokines and relevant pro-angiogenic factors was assessed between wild-type and FPR1-deficiency OIR mice. The impact of FPR1 on retinal angiogenesis was evaluated through quantifying retinal vaso-obliteration and neovascularization between and OIR mice. At last, the neuronal effect of FPR1 on the ischemic retina was investigated by ERG between wild-type and FPR1-deficient OIR mice.
The expression of FPR1 significantly increased in the retina of OIR. Furthermore, FPR1 deficiency downregulated pro-inflammatory and pro-angiogenic factors. Ablation of FPR1 suppressed the retinal pathological neovascularization and promoted reparative revascularization, ultimately improving retinal neural function after ischemic injury.
In ischemic retinopathy, FPR1 aggravates inflammation and inhibits reparative angiogenesis to exacerbate neuronal dysfunction.
缺血性视网膜病变是威胁视力的主要原因。炎症在缺血性视网膜病变的发病机制中起重要作用。甲酰肽受体 1（FPR1）已被报道参与炎症性疾病的调节。然而，FPR1 在缺血性视网膜损伤进展中的作用尚未得到充分解释。
通过实时 PCR 和 Western blot 在 OIR 视网膜中测量 FPR1 的激活。在野生型和 FPR1 缺陷型 OIR 小鼠之间评估 FPR1 对炎症细胞因子和相关促血管生成因子表达的影响。通过量化 和 OIR 小鼠之间的视网膜血管闭塞和新生血管化来评估 FPR1 对视网膜血管生成的影响。最后，通过野生型和 FPR1 缺陷型 OIR 小鼠之间的 ERG 研究 FPR1 对缺血性视网膜的神经元影响。
FPR1 在 OIR 视网膜中的表达显著增加。此外，FPR1 缺乏下调促炎和促血管生成因子。FPR1 缺失抑制视网膜病理性新生血管形成，促进修复性血管生成，最终改善缺血性损伤后的视网膜神经功能。
在缺血性视网膜病变中，FPR1 加重炎症并抑制修复性血管生成，从而加剧神经元功能障碍。
