The positive feedback loop of the NAT10/Mybbp1a/p53 axis promotes cardiomyocyte ferroptosis to exacerbate cardiac I/R injury

Qu, Zhezhe; Pang, Xiaochen; Mei, Zhongting; Li, Ying; Zhang, Yaozhi; Huang, Chuanhao; Liu, Kuiwu; Yu, Shuting; Wang, Changhao; Sun, Zhiyong; Liu, Yingqi; Li, Xin; Jia, Yingqiong; Dong, Yuechao; Lu, Meixi; Ju, Tiantian; Wu, Fan; Huang, Min; Li, Na; Dou, Shunkang; Jiang, Jianhao; Dong, Xianhui; Zhang, Yi; Li, Wanhong; Yang, Baofeng; Du, Weijie

doi:10.1016/j.redox.2024.103145

Redox Biology

2024

DOI: 10.1016/j.redox.2024.103145

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The positive feedback loop of the NAT10/Mybbp1a/p53 axis promotes cardiomyocyte ferroptosis to exacerbate cardiac I/R injury

Zhezhe Qu,

Xiaochen Pang,

Zhongting Mei

et al.

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Cited by 7 publications

References 48 publications

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The role and mechanism of NAT10‐mediated ac4C modification in tumor development and progression

Gu,

Zou,

Pan

et al. 2024

MedComm

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RNA modification has emerged as a crucial area of research in epigenetics, significantly influencing tumor biology by regulating RNA metabolism. N‐acetyltransferase 10 (NAT10)‐mediated N4‐acetylcytidine (ac4C) modification, the sole known acetylation in eukaryotic RNA, influences cancer pathogenesis and progression. NAT10 is the only writer of ac4C and catalyzes acetyl transfer on targeted RNA, and ac4C helps to improve the stability and translational efficiency of ac4C‐modified RNA. NAT10 is highly expressed and associated with poor prognosis in pan‐cancers. Based on its molecular mechanism and biological functions, ac4C is a central factor in tumorigenesis, tumor progression, drug resistance, and tumor immune escape. Despite the increasing focus on ac4C, the specific regulatory mechanisms of ac4C in cancer remain elusive. The present review thoroughly analyzes the current knowledge on NAT10‐mediated ac4C modification in cancer, highlighting its broad regulatory influence on targeted gene expression and tumor biology. This review also summarizes the limitations and perspectives of current research on NAT10 and ac4C in cancer, to identify new therapeutic targets and advance cancer treatment strategies.

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The role and mechanism of NAT10‐mediated ac4C modification in tumor development and progression

Gu,

Zou,

Pan

et al. 2024

MedComm

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Ilexgenin A Alleviates Myocardial Ferroptosis in Response to Ischemia Reperfusion Injury via the SIRT1 Pathway

Yang,

Jue,

Luo

et al. 2024

Phytotherapy Research

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Myocardial ischemia–reperfusion (I/R) injury has emerged as an increasingly serious cardiovascular health concern worldwide, with ferroptosis playing a pivotal role as the underlying pathogenic process. This study aimed to investigate the pharmacological effect and mechanism of Ilexgenin A on cardiomyocyte ferroptosis induced by myocardial I/R injury. In vivo, we established a murine anterior descending artery ligation/recanalization model to evaluate the cardioprotective effect of Ilexgenin A. Bioinformatics analysis, molecular docking, and Surface Plasmon Resonance imaging were conducted to predict the pharmacological targets of Ilexgenin A. In vitro experiments, the neonatal rat cardiomyocytes (NRCMs) were utilized to further explore the mechanism of Ilexgenin A in inhibiting ferroptosis using chemiluminescence and immunofluorescence staining, electron microscopy, biochemical assay, RT‐qPCR, western blotting, and so on. The results showed that Ilexgenin A protected against cardiac dysfunction, ameliorated myocardial ferroptosis and mitochondrial damage induced by murine myocardial I/R injury via the silence information regulator 1 (SIRT1) pathway, the trend was consistently observed in NRCMs. Additionally, the SIRT1 knockdown by siRNA delivery partially abrogated the beneficial effects of Ilexgenin A on ameliorating mitochondrial damage, and then aggravated erastin‐induced ferroptosis in NRCMs. Overall, Our research demonstrated that the inhibition of ferroptosis via the SIRT1 pathway was one of the mechanisms by which Ilexgenin A exerted cardioprotective effect.

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Improvement of MASLD and MASH by suppression of hepatic N-acetyltransferase 10

Yang,

Lu,

Liu

et al. 2024

Molecular Metabolism

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The positive feedback loop of the NAT10/Mybbp1a/p53 axis promotes cardiomyocyte ferroptosis to exacerbate cardiac I/R injury

Cited by 7 publications

References 48 publications

The role and mechanism of NAT10‐mediated ac4C modification in tumor development and progression

The role and mechanism of NAT10‐mediated ac4C modification in tumor development and progression

Ilexgenin A Alleviates Myocardial Ferroptosis in Response to Ischemia Reperfusion Injury via the SIRT1 Pathway

Improvement of MASLD and MASH by suppression of hepatic N-acetyltransferase 10

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