Corrigendum: A novel N-arylpyridone compound alleviates the inflammatory and fibrotic reaction of silicosis by inhibiting the ASK1-p38 pathway and regulating macrophage polarization

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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