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缺血再灌注增加小鼠视网膜中 TRPM7 的表达。

Ischemia-Reperfusion Increases TRPM7 Expression in Mouse Retinas.

机构信息

Departamento de Fisiología, Genética y Microbiología, Universidad de Alicante, 03690 San Vicente del Raspeig, Alicante, Spain.

Departamento de Óptica, Farmacología y Anatomía, Universidad de Alicante, 03690 San Vicente del Raspeig, Alicante, Spain.

出版信息

Int J Mol Sci. 2023 Nov 8;24(22):16068. doi: 10.3390/ijms242216068.

DOI:10.3390/ijms242216068
PMID:38003256
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10671235/
Abstract

Ischemia is the main cause of cell death in retinal diseases such as vascular occlusions, diabetic retinopathy, glaucoma, or retinopathy of prematurity. Although excitotoxicity is considered the primary mechanism of cell death during an ischemic event, antagonists of glutamatergic receptors have been unsuccessful in clinical trials with patients suffering ischemia or stroke. Our main purpose was to analyze if the transient receptor potential channel 7 (TRPM7) could contribute to retinal dysfunction in retinal pathologies associated with ischemia. By using an experimental model of acute retinal ischemia, we analyzed the changes in retinal function by electroretinography and the changes in retinal morphology by optical coherence tomography (OCT) and OCT-angiography (OCTA). Immunohistochemistry was performed to assess the pattern of TRPM7 and its expression level in the retina. Our results show that ischemia elicited a decrease in retinal responsiveness to light stimuli along with reactive gliosis and a significant increase in the expression of TRPM7 in Müller cells. TRPM7 could emerge as a new drug target to be explored in retinal pathologies associated with ischemia.

摘要

缺血是视网膜疾病（如血管阻塞、糖尿病性视网膜病变、青光眼或早产儿视网膜病变）中细胞死亡的主要原因。尽管兴奋性毒性被认为是缺血事件中细胞死亡的主要机制，但谷氨酸能受体拮抗剂在缺血或中风患者的临床试验中并未成功。我们的主要目的是分析瞬时受体电位通道 7（TRPM7）是否会导致与缺血相关的视网膜病变中的视网膜功能障碍。通过使用急性视网膜缺血实验模型，我们通过视网膜电图分析了视网膜功能的变化，并通过光学相干断层扫描（OCT）和 OCT 血管造影（OCTA）分析了视网膜形态的变化。进行免疫组织化学染色以评估 TRPM7 的模式及其在视网膜中的表达水平。我们的结果表明，缺血引起视网膜对光刺激的反应性降低，同时伴有胶质细胞反应性增生和 Müller 细胞中 TRPM7 的表达显著增加。TRPM7 可能成为与缺血相关的视网膜病变中有待探索的新药物靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33d5/10671235/96be13e3fa03/ijms-24-16068-g006.jpg
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2
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J Clin Med. 2023 Mar 21;12(6):2406. doi: 10.3390/jcm12062406.
3
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Int J Mol Sci. 2024 Apr 30;25(9):4877. doi: 10.3390/ijms25094877.
Asia Pac J Ophthalmol (Phila). 2023;12(2):196-210. doi: 10.1097/APO.0000000000000598. Epub 2023 Feb 14.
4
Sevoflurane participates in the protection of rat renal ischemia-reperfusion injury by down-regulating the expression of TRPM7.七氟醚通过下调 TRPM7 的表达参与大鼠肾缺血再灌注损伤的保护。
Immun Inflamm Dis. 2023 Jan;11(1):e753. doi: 10.1002/iid3.753.
5
Retinopathy of prematurity: A review of pathophysiology and signaling pathways.早产儿视网膜病变：病理生理学和信号通路综述。
Surv Ophthalmol. 2023 Mar-Apr;68(2):175-210. doi: 10.1016/j.survophthal.2022.11.007. Epub 2022 Nov 23.
6
Retinal TRP channels: Cell-type-specific regulators of retinal homeostasis and multimodal integration.视网膜 TRP 通道：视网膜内稳态和多模态整合的细胞类型特异性调节剂。
Prog Retin Eye Res. 2023 Jan;92:101114. doi: 10.1016/j.preteyeres.2022.101114. Epub 2022 Sep 24.
7
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