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Ascorbate peroxidase (APX), a type I heme peroxidase, catalyzes oxidation of ascorbic acid. It possesses a high degree of specificity to ascorbic acid. APX gene cluster consists of four sub-clusters: the gene clusters of cytosol, chloroplast, mitochondria, and peroxidase. As a key component of hydrogen peroxide detoxification system, the ascorbate-glutathione cycle, APX plays a vital role in the metabolism of H2O2 of plant cells. Studies showed that APX is one of the most important enzymes, which modulate the cellular H2O2 level in redox signaling system. The expression mechanisms of APX isoenzymes are quite complex. Briefly, cytosolic APX is regulated by a variety of signals; two chloroplastic APX isoenzymes are tissue-dependently regulated by alternative splicing. Generated APXs could regulate redox signaling in cells, which further boosts plants tolerance to abiotic stresses. This review focuses on recent advances concerning catalytic prop-erties, physiological function, and gene expressing regulation and abio-stress responding mechanism of APX.

Purpose The molecular mechanisms and signal pathways of ferroptosis in hepatoblastoma (HB) have not yet been clarified. In previous studies, activating transcription factor 3 (ATF3) was reported to be correlated with several tumors, but the clinical significance of ATF3 has never been determined. Herein, we investigated the clinicopathological value and mechanisms of ATF3 in regulating ferroptosis in HB. Methods The mRNA microarray and RNA-sequencing data of 402 samples from our hospital and public databases were used to estimate ATF3 expression and assess its clinical role in HB. The standard mean difference (SMD) and summary receiver operating characteristic curves were utilized to judge the discrimination ability of ATF3 between HB and non-HB liver tissues. We examined the expression variation of ATF3 in HB cells after the treatment with erastin. We also predicted the target genes of ATF3 as a transcriptional factor from public Chromatin Immunoprecipitation-sequencing data and selected the ferroptosis-related genes for a signaling pathway analysis. Results In ten series, the pooled SMD for ATF3 was −0.91, demonstrating that ATF3 expression was predominantly lower in HB than in non-HB liver tissues. ATF3 down-regulation showed moderate potential to distinguish HB from non-HB liver tissues (area under curves = 0.83, 95% confidence interval = 0.79–0.86). Altogether, 4855 putative targets of ATF3 as a transcriptional factor were collected, among which, 60 genes were ferroptosis-related. Conclusion The down-regulated ATF3 expression may play a vital role in the occurrence of HB possible partially by regulating ferroptosis.