A Novel N-Arylpyridone Compound Alleviates the Inflammatory and Fibrotic Reaction of Silicosis by Inhibiting the ASK1-p38 Pathway and Regulating Macrophage Polarization
- 1Department of Respiratory Medicine, The Second Hospital of Jilin University, Jilin, China
- 2Department of Pulmonary and Critical Care Medicine Center of Respiratory Medicine, China-Japan Friendship Hospital, Capital Medical University, National Center for Respiratory Medicine, National Clinical Research Center for Respiratory Diseases, Institute of Respiratory Medicine, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China
- 3Department of Pulmonary and Critical Care Medicine, China-Japan Friendship School of Clinical Medicine, Peking University, Beijing, China
- 4Institute of Clinical Medical Sciences, China-Japan Friendship Hospital, Beijing, China
- 5State Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Beijing, China
by Fan M, Xiao H, Song D, Zhu L, Zhang J, Zhang X, Wang J, Dai H and Wang C (2022). Front. Pharmacol. 13:848435. doi: 10.3389/fphar.2022.848435
In the original article, there was a mistake in the legend for Figure 9 as published. The labelling of Figure 9 with macrophages is misleading as we used a RAW264.7 macrophage cell line. The correct legend appears below:
FIGURE 9
AKEX0011 inhibited RAW264.7 from secreting pro-inflammatory cytokines, blocked p38 MAPK signaling, and reduced silica-induced apoptosis and M1 polarization. There were eight cell groups: PBS Control (abbreviated as “Control” in the graphs), PBS + AKEX0011 (200 μg/ml) (abbreviated as “AKEX”), Silica pre, Silica pre + AKEX0011 (100 μg/ml) (abbreviated as “Si pre + AKEX L”), and Silica pre + AKEX0011 (200 μg/ml) (abbreviated as “Si pre + AKEX H”), Silica post, Silica post + AKEX0011 (100 μg/ml) (abbreviated as “Si post + AKEX L”), and Silica post + AKEX0011 (200 μg/ml) (abbreviated as “Si post + AKEX H”). (A−D) IL-6 IL-1β, TNF-α, and TGF-β in cell supernatant detected by ELISA (n = 3). (E) Apoptosis (Annexin V+/PI− and Annexin V+/PI+) detection by FACS in each experimental group. (F–H) WB and quantification of P-p38, p38, P-ASK1, and ASK1. β-actin was used as a loading control. (I–J) M1 (F4/80 + CD86+) and M2 (F4/80 + CD163+) macrophage proportions detected by FACS in RAW264.7 and statistical analysis (n = 3). (K) WB of iNOS P-p65 p65. (L, N) Quantification of band densities fromWB images in (k), (n = 3). (M) mRNA levels of iNOS in lung tissues detected by qPCR (n = 3). All data were presented as mean ± SEM; *p < .05, **p < .01, ***p < .001, and ****p < .0001.
The authors apologize for this error and state that this does not change the scientific conclusions of the article in any way. The original article has been updated.
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Keywords: silicosis, pulmonary fibrosis, AKEX0011, macrophage polarization, pirfenidone
Citation: Fan M, Xiao H, Song D, Zhu L, Zhang J, Zhang X, Wang J, Dai H and Wang C (2023) Corrigendum: A novel N-arylpyridone compound alleviates the inflammatory and fibrotic reaction of silicosis by inhibiting the ASK1-p38 pathway and regulating macrophage polarization. Front. Pharmacol. 13:1109002. doi: 10.3389/fphar.2022.1109002
Received: 27 November 2022; Accepted: 12 December 2022;
Published: 18 January 2023.
Edited and reviewed by:
Dieter Steinhilber, Goethe University Frankfurt, GermanyCopyright © 2023 Fan, Xiao, Song, Zhu, Zhang, Zhang, Wang, Dai and Wang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
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