Department of Pharmacology, Chiba University Graduate School of Medicine, 1-8-1, Inohana, Chuo-ku, Chiba-shi 260-8670, Chiba, Japan.
Department of Neuropharmacology, Interdisciplinary Graduate School of Medicine, University of Yamanashi, 1110 Shimokato, Chuo 409-3898, Yamanashi, Japan.
Molecules. 2022 Jun 7;27(12):3655. doi: 10.3390/molecules27123655.
A sub-lethal ischemic episode (preconditioning [PC]) protects neurons against a subsequent lethal ischemic injury. This phenomenon is known as ischemic tolerance. PC itself does not cause brain damage, but affects glial responses, especially astrocytes, and transforms them into an ischemia-resistant phenotype. P2X7 receptors (P2X7Rs) in astrocytes play essential roles in PC. Although P2X7Rs trigger inflammatory and toxic responses, PC-induced P2X7Rs in astrocytes function as a switch to protect the brain against ischemia. In this review, we focus on P2X7Rs and summarize recent developments on how astrocytes control P2X7Rs and what molecular mechanisms they use to induce ischemic tolerance.
亚致死性缺血发作（预处理 [PC]）可保护神经元免受随后的致死性缺血损伤。这种现象被称为缺血耐受。PC 本身不会造成脑损伤，而是影响神经胶质反应，特别是星形胶质细胞，并将其转化为抗缺血表型。星形胶质细胞中的 P2X7 受体（P2X7Rs）在 PC 中起着重要作用。尽管 P2X7Rs 引发炎症和毒性反应，但 PC 诱导的星形胶质细胞中的 P2X7Rs 起着保护大脑免受缺血的作用。在这篇综述中，我们重点介绍 P2X7Rs，并总结星形胶质细胞如何控制 P2X7Rs 以及它们使用哪些分子机制来诱导缺血耐受的最新进展。
