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1
Corrigendum: Activation of A2A receptor by PDRN reduces neuronal damage and stimulates WNT/β-catenin driven neurogenesis in spinal cord injury.勘误：PDRN激活A2A受体可减少脊髓损伤中的神经元损伤并刺激WNT/β-连环蛋白驱动的神经发生。
Front Pharmacol. 2022 Nov 3;13:1073726. doi: 10.3389/fphar.2022.1073726. eCollection 2022.
2
Activation of A2A Receptor by PDRN Reduces Neuronal Damage and Stimulates WNT/β-CATENIN Driven Neurogenesis in Spinal Cord Injury.PDRN激活A2A受体可减轻脊髓损伤中的神经元损伤并刺激WNT/β-连环蛋白驱动的神经发生。
Front Pharmacol. 2018 May 29;9:506. doi: 10.3389/fphar.2018.00506. eCollection 2018.
3
PDRN, a Bioactive Natural Compound, Ameliorates Imiquimod-Induced Psoriasis through NF-κB Pathway Inhibition and Wnt/β-Catenin Signaling Modulation.PDRN，一种生物活性天然化合物，通过抑制 NF-κB 通路和调节 Wnt/β-连环蛋白信号通路改善咪喹莫特诱导的银屑病。
Int J Mol Sci. 2020 Feb 12;21(4):1215. doi: 10.3390/ijms21041215.
4
Corrigendum: Polydeoxyribonucleotide, an adenosine-A2 receptor agonist, preserves blood testis barrier from cadmium-induced injury.勘误：聚脱氧核糖核苷酸，一种腺苷 A2 受体激动剂，可保护血睾屏障免受镉诱导的损伤。
Front Pharmacol. 2022 Nov 16;13:1073543. doi: 10.3389/fphar.2022.1073543. eCollection 2022.
5
Corrigendum: Adenosine receptor stimulation by polydeoxyribonucleotide improves tissue repair and symptomology in experimental colitis.勘误：多聚脱氧核糖核苷酸刺激腺苷受体可改善实验性结肠炎的组织修复和症状。
Front Pharmacol. 2022 Nov 10;13:1073445. doi: 10.3389/fphar.2022.1073445. eCollection 2022.
6
PDRN, a natural bioactive compound, blunts inflammation and positively reprograms healing genes in an "in vitro" model of oral mucositis.PDRN，一种天然生物活性化合物，在口腔黏膜炎的“体外”模型中能减轻炎症并积极重编程愈合基因。
Biomed Pharmacother. 2021 Jun;138:111538. doi: 10.1016/j.biopha.2021.111538. Epub 2021 Mar 31.
7
Adenosine A2A receptor agonist polydeoxyribonucleotide ameliorates short-term memory impairment by suppressing cerebral ischemia-induced inflammation via MAPK pathway.腺嘌呤 A2A 受体激动剂聚脱氧核糖核苷酸通过 MAPK 通路抑制脑缺血诱导的炎症改善短期记忆障碍。
PLoS One. 2021 Mar 18;16(3):e0248689. doi: 10.1371/journal.pone.0248689. eCollection 2021.
8
Polydeoxyribonucleotide Exerts Protective Effect Against CCl-Induced Acute Liver Injury Through Inactivation of NF-κB/MAPK Signaling Pathway in Mice.多聚脱氧核苷酸通过抑制 NF-κB/MAPK 信号通路对 CCl4 诱导的小鼠急性肝损伤发挥保护作用。
Int J Mol Sci. 2020 Oct 24;21(21):7894. doi: 10.3390/ijms21217894.
9
Adenosine A Receptor Agonist Polydeoxyribonucleotide Alleviates Interstitial Cystitis-Induced Voiding Dysfunction by Suppressing Inflammation and Apoptosis in Rats.腺苷 A 受体激动剂聚脱氧核糖核苷酸通过抑制大鼠炎症和细胞凋亡减轻间质性膀胱炎诱导的排尿功能障碍。
J Inflamm Res. 2021 Feb 15;14:367-378. doi: 10.2147/JIR.S287346. eCollection 2021.
10
Protective Effect of Polydeoxyribonucleotide Against CCl4-Induced Acute Liver Injury in Mice.聚脱氧核糖核苷酸对四氯化碳诱导的小鼠急性肝损伤的保护作用
Int Neurourol J. 2020 Nov;24(Suppl 2):88-95. doi: 10.5213/inj.2040430.215. Epub 2020 Nov 23.

引用本文的文献

1
Decellularized tissue matrices hydrogels functionalized with extracellular vesicles promote macrophage reprogramming and neural stem cell differentiation for spinal cord injury repair.用细胞外囊泡功能化的脱细胞组织基质水凝胶可促进巨噬细胞重编程和神经干细胞分化，用于脊髓损伤修复。
J Nanobiotechnology. 2025 Feb 25;23(1):139. doi: 10.1186/s12951-025-03152-0.

勘误：PDRN激活A2A受体可减少脊髓损伤中的神经元损伤并刺激WNT/β-连环蛋白驱动的神经发生。

Corrigendum: Activation of A2A receptor by PDRN reduces neuronal damage and stimulates WNT/β-catenin driven neurogenesis in spinal cord injury.

作者信息

Irrera Natasha, Arcoraci Vincenzo, Mannino Federica, Vermiglio Giovanna, Pallio Giovanni, Minutoli Letteria, Bagnato Gianluca, Anastasi Giuseppe Pio, Mazzon Emanuela, Bramanti Placido, Squadrito Francesco, Altavilla Domenica, Bitto Alessandra

机构信息

Department of Clinical and Experimental Medicine, AOU Policlinico G. Martino, University of Messina, Messina, Italy.

Department of Biomedical and Dental Sciences and Morphological and Functional Sciences, AOU Policlinico G. Martino, University of Messina, Messina, Italy.

出版信息

Front Pharmacol. 2022 Nov 3;13:1073726. doi: 10.3389/fphar.2022.1073726. eCollection 2022.

DOI:10.3389/fphar.2022.1073726
PMID:36408237
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9671133/
Abstract

[This corrects the article DOI: 10.3389/fphar.2018.00506.].

摘要

[本文更正了文章的数字对象标识符：10.3389/fphar.2018.00506。]