期刊：
FRONTIERS IN CELLULAR AND INFECTION MICROBIOLOGY,2023年13:1179369 ISSN：2235-2988
通讯作者：
Li, Dan;Tang, SY;Li, D
作者机构：
[Li, Dan; Tang, Si-Yuan; Li, D] Cent South Univ, Xiangya Sch Nursing, Changsha, Hunan, Peoples R China.;[Li, D; Li, Dan] Hunan Open Univ, Coll Appl Technol, Changsha, Hunan, Peoples R China.;[Lei, Sheng] Hunan Chest Hosp, Intervent Radiol Ctr, Changsha, Hunan, Peoples R China.;[Xie, He-Bin] Univ South China, Changsha Cent Hosp, Dept Drug Clin Trial Inst, Hengyang Med Sch, Changsha, Hunan, Peoples R China.;[Li, Lin-Qi] Univ South China, Sch Publ Hlth, Hengyang, Peoples R China.
通讯机构：
[Li, D ] H;[Tang, SY ; Li, D] C;Cent South Univ, Xiangya Sch Nursing, Changsha, Hunan, Peoples R China.;Hunan Open Univ, Coll Appl Technol, Changsha, Hunan, Peoples R China.
摘要：
Slc39a10 (Zip10), as a zinc transporter, plays an essential role in the survival of fetal hematopoietic stem/progenitor cells in both zebrafish and mice. Loss of Slc39a10 causes impaired hematopoiesis that can be rescued by zinc supplementation or inhibiting necroptosis. This study shows that Slc39a10 promotes the development of fetal hematopoietic stem cells by maintaining zinc homeostasis. Abstract The role of zinc in hematopoiesis is currently unclear. Here, SLC39A10 (ZIP10) is identified as a key zinc transporter in hematopoiesis. The results show that in zebrafish, Slc39a10 is a key regulator of the response to zinc deficiency. Surprisingly, both slc39a10 mutant zebrafish and hematopoietic Slc39a10‐deficient mice develop a more severe form of impaired hematopoiesis than animals lacking transferrin receptor 1, a well‐characterized iron gatekeeper, indicating that zinc plays a larger role than iron in hematopoiesis, at least in early hematopoietic stem cells (HSCs). Furthermore, it is shown that loss of Slc39a10 causes zinc deficiency in fetal HSCs, which in turn leads to DNA damage, apoptosis, and G1 cell cycle arrest. Notably, zinc supplementation largely restores colony formation in HSCs derived from hematopoietic Slc39a10‐deficient mice. In addition, inhibiting necroptosis partially restores hematopoiesis in mouse HSCs, providing mechanistic insights into the requirement for zinc in mediating hematopoiesis. Together, these findings indicate that SLC39A10 safeguards hematopoiesis by protecting against zinc deficiency‐induced necroptosis, thus providing compelling evidence that SLC39A10 and zinc homeostasis promote the development of fetal HSCs. Moreover, these results suggest that SLC39A10 may serve as a novel therapeutic target for treating anemia and zinc deficiency‐related disorders.
通讯机构：
[Lili Chen] D;Department of Public Health Laboratory Sciences, School of Public Health, Hengyang Medical School, University of South China, Hengyang, China<&wdkj&>Hunan Key Laboratory of Typical Environmental Pollution and Health Hazards, School of Public Health, Hengyang Medical School, University of South China, Hengyang, China<&wdkj&>Hengyang Engineering Technology Research Center, Hengyang, China
摘要：
Helicobacter pylori is a kind of Gram-negative bacteria that parasitizes on human gastric mucosa. Helicobacter pylori infection is very common in human beings, which often causes gastrointestinal diseases, including chronic gastritis, duodenal ulcer and gastric cancer. MicroRNAs are a group of endogenous non-coding single stranded RNAs, which play an important role in cell proliferation, differentiation, autophagy, apoptosis and inflammation. In recent years, relevant studies have found that the expression of microRNA is changed after Helicobacter pylori infection, and then regulate the biological process of host cells. This paper reviews the regulation role of microRNAs on cell biological behavior through different signal pathways after Helicobacter pylori infection.
期刊：
Journal of Applied Toxicology,2023年43(8):1169-1182 ISSN：0260-437X
通讯作者：
Zhaohui Zhang
作者机构：
[Zhang, Zhaohui; Liu, Xiaodong; Jin, Huiyun; Zhang, Linfang; Chen, Shaoxiong; Liu, Xiuli; Li, Guilan] Univ South China, Sch publ Hlth, Hengyang Med Sch, Dept Prevent Med, Hengyang 421001, Hunan, Peoples R China.;[Zhang, Zhaohui; Liu, Xiaodong; Jin, Huiyun; Chen, Shaoxiong; Liu, Xiuli; Li, Guilan] Univ South China, Hengyang Med Sch, Hunan Prov Key Lab Typ Environm Pollut & Hlth Haza, Hengyang 421001, Hunan, Peoples R China.
通讯机构：
[Zhaohui Zhang] D;Department of Preventive Medicine, School of public health, Hengyang Medical School, University of South China, Hengyang, Hunan, 421001 China<&wdkj&>Hunan Province Key Laboratory of Typical Environmental Pollution and Health Hazards, Hengyang Medical School, University of South China, Hengyang, Hunan, 421001 China
摘要：
Beryllium sulfate (BeSO4) can result to lung injuries, such as leading to lipid peroxidation and autophagy, and the treatment of beryllium disease has not been well improved. Ferroptosis is a regulated cell death process driven by iron-dependent and lipid peroxidation, while ferritinophagy is a process mediated by nuclear receptor coactivator 4 (NCOA4), combined with ferritin heavy chain 1 (FTH1) degradation and release Fe2+, which regulated intracellular iron metabolism and ferroptosis. Hydrogen sulfide (H2S) has the effects of antioxidant, antiautophagy, and antiferroptosis. This study aimed to investigate the effect of H2S on BeSO4-induced ferroptosis and ferritinophagy in 16HBE cells and the underlying mechanism. In this study, BeSO4-induced 16HBE cell injury model was established based on cellular level and pretreated with deferoxamine (DFO, a ferroptosis inhibitor), sodium hydrosulfide (NaHS, a H2S donor), or NCOA4 siRNA and, subsequently, performed to detect the levels of lipid peroxidation and Fe2+ and the biomarkers of ferroptosis and ferritinophagy. More importantly, our research found that DFO, NaHS, or NCOA4 siRNA alleviated BeSO4-induced ferroptosis and ferritinophagy by decreasing the accumulation of Fe2+ and lipid peroxides. Furthermore, the relationship between ferroptosis, ferritinophagy, H2S, and beryllium disease is not well defined; therefore, our research is innovative. Overall, our results provided a new theoretical basis for the prevention and treatment of beryllium disease and suggested that the application of H2S, blocking ferroptosis, and ferritinophagy may be a potential therapeutic direction for the prevention and treatment of beryllium disease.
摘要：
Microcystin-LR (MC-LR) contamination is a worldwide environmental problem that poses a grave threat to the water ecosystem and public health. Exposure to MC-LR has been associated with the development of intestinal injury, but there are no effective treatments for MC-LR-induced intestinal disease. Probiotics are "live microorganisms that are beneficial to the health of the host when administered in sufficient quantities". It has been demonstrated that probiotics can prevent or treat a variety of human diseases; however, their ability to mitigate MC-LR-induced intestinal harm has not yet been investigated. The objective of this study was to determine whether probiotics can mitigate MC-LR-induced intestinal toxicity and its underlying mechanisms. We first evaluated the pathological changes in colorectal tissues using an animal model with sub-chronic exposure to low-dose MC-LR, HE staining to assess colorectal histopathologic changes, qPCR to detect the expression levels of inflammatory factors in colorectal tissues, and WB to detect the alterations on CSF1R signaling pathway proteins in colorectal tissues. Microbial sequencing analysis and screening of fecal microorganisms differential to MC-LR treatment in mice. To investigate the role of microorganisms in MC-LR-induced colorectal injury, an in vitro model of MC-LR co-treatment with microorganisms was developed. Our findings demonstrated that MC-LR treatment induced an inflammatory response in mouse colorectal tissues, promoted the expression of inflammatory factors, activated the CSF1R signaling pathway, and significantly decreased the abundance of Lactobacillus. In a model of co-treatment with MC-LR and Lactobacillus fermentum (L. fermentum), it was discovered that L. fermentum substantially reduced the incidence of the colorectal inflammatory response induced by MC-LR and inhibited the protein expression of the CSF1R signaling pathway. This is the first study to suggest that L. fermentum inhibits the CSF1R signaling pathway to reduce the incidence of MC-LR-induced colorectal inflammation. This research may provide an excellent experimental foundation for the development of strategies for the prevention and treatment of intestinal diseases in MC-LR.
摘要：
Ionizing radiation (IR) can induce pulmonary fibrosis by causing epithelial mesenchymal transition (EMT), but the exact mechanism has not been elucidated. To investigate the molecular mechanism of how radiation induces pulmonary fibrosis by altering miR-486-3p content and thus inducing EMT. The changes of miR-486-3p in cells after irradiation were detected by RT-qPCR. Western blot was used to detect the changes of cellular epithelial marker protein E-cadherin, mesenchymal marker N-cadherin, Vimentin and other proteins. The target gene of miR-486-3p was predicted by bioinformatics method and the binding site was verified by dual luciferase reporter system. In vivo experiments, adeno-associated virus (AAV) was used to carry miR-486-3p mimic to lung. Radiation-induced pulmonary fibrosis (RIPF) model was constructed by 25Gy60Co γ-rays. The structural changes of mouse lung were observed by HE and Masson staining. The expression of relevant proteins in mice was detected by immunohistochemistry. IR could decrease the miR-486-3p levels in vitro and in vivo, and that effect was closely correlated to the occurrence of RIPF. The expression of Snail, which induces EMT, was shown to be restrained by miR-486-3p. Therefore, knockdown of Snail blocked the EMT process induced by radiation or knockdown of miR-486-3p. In addition, the molecular mechanism underlying the IR-induced miRNA level reduction was explored. The increased in BCL6 could inhibit the formation of pri-miR-486-3p, thereby reducing the levels of miR-486-3p in the alveolar epithelial cells, which would otherwise promote EMT and contribute to RIPF by targeting Snail. IR can exacerbate RIPF in mice by activating the transcription factor BCL6, which inhibits the transcription of miR-486-3p and decreases its content, which in turn increases the content of the target gene slug and triggers EMT.
期刊：
Journal of Hazardous Materials,2022年440:129793 ISSN：0304-3894
通讯作者：
Fei Yang
作者机构：
[Feng, Xiangling; Chen, Jihua; Liu, Wenya; Yang, Fei; Yang, Yue; Chen, Mengshi] Cent South Univ, Xiangya Sch Publ Hlth, Hunan Prov Key Lab Clin Epidemiol, Changsha, Peoples R China.;[Wang, Hui; Deng, Shuxiang; Chu, Hanyu; Cao, Yi; Liu, Ying; Long, Dingxin; Cai, Danping; Cao, Deliang; Yang, Fei] Univ South China, Sch Publ Hlth, Hengyang Med Sch, Hunan Prov Key Lab Typ Environm Pollut & Hlth Haza, Hengyang, Peoples R China.;[Wang, Xiaoyan] Cent South Univ, Xiangya Hosp 3, Dept Gastroenterol, Changsha, Peoples R China.;[Chen, Ling] Univ South China, Affiliated Hosp 1, Hengyang Med Sch, Hengyang, Peoples R China.;[Wang, Chengkun] Univ South China, Sch Basic Med, Hengyang Med Sch, Dept Med Pathol, Hengyang, Peoples R China.
通讯机构：
[Fei Yang] H;Hunan Province Key Laboratory of Typical Environmental Pollution and Health Hazards, School of Public Health, Hengyang Medical School, University of South China, Hengyang, China<&wdkj&>Hunan Provincial Key Laboratory of Clinical Epidemiology, Xiangya School of Public Health, Central South University, Changsha, China<&wdkj&>Key Laboratory of Environmental Medicine Engineering, Ministry of Education, School of Public Health, Southeast University, Nanjing, China
摘要：
Microcystin-LR (MC-LR) is a very common toxic cyanotoxins threating ecosystems and the public health. This study aims to explore the long-term effects and potential toxicity mechanisms of MC-LR exposure at environmental levels on colorectal injury. We performed histopathological, biochemical indicator and multi-omics analyses in mice with low-dose MC-LR exposure for 12 months. Long-term environmental levels of MC-LR exposure caused epithelial barrier disruption, inflammatory cell infiltration and an increase of collagen fibers in mouse colorectum. Integrated proteotranscriptomics revealed differential expression of genes/proteins, including CSF1R, which were mainly involved in oxidative stress-induced premature senescence and inflammatory response. MC-LR induced chronic inflammation and fibrosis through oxidative stress and CSF1R/Rap1b signaling pathway were confirmed in cell models. We found for the first time that long-term environmental levels of MC-LR exposure caused colorectal chronic inflammation, fibrosis and barrier disruption via a novel CSF1R/Rap1b signaling pathway. Moreover, MC-LR changed the gut microbiota and microbial-related metabolites in a vicious cycle aggravating colorectal injury. These findings provide novel insights into the effects and toxic mechanisms of MC-LR and suggest strategies for the prevention and treatment of MC-caused intestinal diseases.
通讯机构：
[Hua Guan; Chen-Jun Bai] D;[Ping-Kun Zhou] C;Department of Radiation Biology, Beijing Key Laboratory for Radiobiology, Beijing Institute of Radiation Medicine, Beijing, People’s Republic of China<&wdkj&>Department of Radiation Biology, Beijing Key Laboratory for Radiobiology, Beijing Institute of Radiation Medicine, Beijing, People’s Republic of China<&wdkj&>College of Public Health, Hengyang Medical School, University of South China, Hengyang, People’s Republic of China<&wdkj&>Department of Radiation Biology, Beijing Key Laboratory for Radiobiology, Beijing Institute of Radiation Medicine, Beijing, People’s Republic of China
关键词：
LPAR5;ERK;Radioresistance;EMT;Radiotherapy
摘要：
BACKGROUND: Epithelial-to-mesenchymal transition (EMT) is a critical event contributing to more aggressive phenotypes in cancer cells. EMT is frequently activated in radiation-targeted cells during the course of radiotherapy, which often endows cancers with acquired radioresistance. However, the upstream molecules driving the signaling pathways of radiation-induced EMT have not been fully delineated. METHODS: In this study, RNA-seq-based transcriptome analysis was performed to identify the early responsive genes of HeLa cells to γ-ray irradiation. EMT-associated genes were knocked down by siRNA technology or overexpressed in HeLa cells and A549 cells, and the resulting changes in phenotypes of EMT and radiosensitivity were assessed using qPCR and Western blotting analyses, migration assays, colony-forming ability and apoptosis of flow cytometer assays. RESULTS: Through RNA-seq-based transcriptome analysis, we found that LPAR5 is downregulated in the early response of HeLa cells to γ-ray irradiation. Radiation-induced alterations in LPAR5 expression were further revealed to be a bidirectional dynamic process in HeLa and A549 cells, i.e., the early downregulating phase at 2 ~ 4h and the late upregulating phase at 24h post-irradiation. Overexpression of LPAR5 prompts EMT programing and migration of cancer cells. Moreover, increased expression of LPAR5 is significantly associated with IR-induced EMT and confers radioresistance to cancer cells. Knockdown of LPAR5 suppressed IR-induced EMT by attenuating the activation of ERK signaling and downstream Snail, MMP1, and MMP9 expression. CONCLUSIONS: LPAR5 is an important upstream regulator of IR-induced EMT that modulates the ERK/Snail pathway. This study provides further insights into understanding the mechanism of radiation-induced EMT and identifies promising targets for improving the effectiveness of cancer radiation therapy.
作者：
Liu, Haohao;Zeng, Xin;Wang, Yueqin;Losiewicz, Michael D.;Chen, Xinghai;...
期刊：
JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY,2022年70(35):10907-10918 ISSN：0021-8561
通讯作者：
Fei Yang<&wdkj&>Huizhen Zhang
作者机构：
[Liu, Haohao; Wang, Yongshui; Guo, Xing; Zhang, Huizhen; Zeng, Xin; Du, Xingde; Yuan, Shumeng; Wang, Yueqin; Zhang, Bingyu] Zhengzhou Univ, Coll Publ Hlth, Zhengzhou 450001, Henan, Peoples R China.;[Yang, Fei] Univ South China, Sch Publ Hlth, Hengyang Med Sch, Hunan Prov Key Lab Typ Environm Pollut & Hlth Haza, Hengyang 421001, Hunan, Peoples R China.;[Yang, Fei] Cent South Univ, Xiangya Sch Publ Hlth, Hunan Prov Key Lab Clin Epidemiol, Changsha 410008, Hunan, Peoples R China.;[Chen, Xinghai; Losiewicz, Michael D.] St Marys Univ, Dept Chem & Biochem, San Antonio, TX 78228 USA.
通讯机构：
[Fei Yang] H;[Huizhen Zhang] C;Hunan Province Key Laboratory of Typical Environmental Pollution and Health Hazards, School of Public Health, Hengyang Medical School, University of South China, Hengyang421001, Hunan, China<&wdkj&>Hunan Provincial Key Laboratory of Clinical Epidemiology, Xiangya School of Public Health, Central South University, Changsha410008, Hunan, China<&wdkj&>College of Public Health, Zhengzhou University, Zhengzhou450001, Henan, China
摘要：
Microcystin-leucine arginine (MC-LR), ubiquitous in water and food, is a threat to public health. In the present study, after C57BL/6J mice were fed with environmental concentrations of MC-LR (0, 1, 30, 60, 90, and 120 μg/L) for 6, 9, and 12 months, it was found that MC-LR could enter into mouse lung tissues and cause microstructural damage, as shown by western blotting and HE staining. Electron microscopy examination showed that MC-LR could damage the lung barrier by disruption of the tight junctions, which was confirmed by the decreased expression of tight junction markers, including Occludin, Claudin1, and ZO-1. In addition, MC-LR also increased the ubiquitination of Claudin1, indicating that MC-LR could disrupt tight junctions by promoting the degradation of Claudin1. Furthermore, MC-LR increased the levels of TNF-α and IL-6 in mouse lung tissues, leading to pneumonia. Importantly, pretreatment with PP2A activator D-erythro-sphingosine (DES) was found to significantly alleviate MC-LR-induced decrease of Occludin and Claudin1 by inhibiting the P-AKT/Snail pathway in vitro. Together, this study revealed that chronic exposure to MC-LR causes lung barrier damage, which involves PP2A activity inhibition and enhancement of Claudin1 ubiquitination. This study broadens the awareness of the toxic effects of MC-LR on the respiratory system, which has deep implications for public health.
作者机构：
[Pan, Jianming; Liu, Bangxiang; Hu, Panwang; Wang, Mengzhu; Niu, Xiangheng; Zhu, Hengjia] Jiangsu Univ, Inst Green Chem & Chem Technol, Sch Chem & Chem Engn, Zhenjiang 212013, Peoples R China.;[Niu, Xiangheng] Univ South China, Sch Publ Hlth, Hengyang Med Sch, Hengyang 421001, Peoples R China.
通讯机构：
[Xiangheng Niu] I;Institute of Green Chemistry and Chemical Technology, School of Chemistry and Chemical Engineering, Jiangsu University, Zhenjiang 212013, China<&wdkj&>School of Public Health, Hengyang Medical School, University of South China, Hengyang 421001, China
作者：
Xiaomin Tang;Fengmei Song;Weichao Zhao;Zhaohui Zhang;Yi Cao
期刊：
Journal of Applied Toxicology,2022年42(11):1822-1831 ISSN：0260-437X
通讯作者：
Zhaohui Zhang<&wdkj&>Yi Cao
作者机构：
[Xiaomin Tang; Fengmei Song; Weichao Zhao; Zhaohui Zhang; Yi Cao] Hunan Province Key Laboratory of Typical Environmental Pollution and Health Hazards, School of Public Health, Hengyang Medical School, University of South China, Hengyang, China
通讯机构：
[Zhaohui Zhang; Yi Cao] H;Hunan Province Key Laboratory of Typical Environmental Pollution and Health Hazards, School of Public Health, Hengyang Medical School, University of South China, Hengyang, China
作者机构：
[Fang, Xuexian] Hangzhou Normal Univ, Sch Publ Hlth, Dept Nutr & Toxicol, State Key Lab Expt Hematol, Hangzhou, Peoples R China.;[Min, Junxia; Wang, Fudi; Fang, Xuexian] Zhejiang Univ, Affiliated Hosp 4, Affiliated Hosp 1,State Key Lab Expt Hematol, Canc Ctr,Sch Med,Inst Translat Med,Sch Publ Hlth, Hangzhou, Peoples R China.;[Wang, Fudi; Fang, Xuexian] Univ South China, Affiliated Hosp 1, Affiliated Hosp 2, Sch Publ Hlth,Basic Med Sci,Hengyang Med Sch, Hengyang, Peoples R China.;[Ardehali, Hossein] Northwestern Univ, Feinberg Cardiovasc & Renal Res Inst, Chicago, IL 60611 USA.
通讯机构：
[Junxia Min; Fudi Wang] T;The Fourth Affiliated Hospital, The First Affiliated Hospital, Institute of Translational Medicine, School of Public Health, Cancer Center, State Key Laboratory of Experimental Hematology, Zhejiang University School of Medicine, Hangzhou, China<&wdkj&>The Fourth Affiliated Hospital, The First Affiliated Hospital, Institute of Translational Medicine, School of Public Health, Cancer Center, State Key Laboratory of Experimental Hematology, Zhejiang University School of Medicine, Hangzhou, China<&wdkj&>The First Affiliated Hospital, The Second Affiliated Hospital, Basic Medical Sciences, School of Public Health, Hengyang Medical School, University of South China, Hengyang, China
通讯机构：
[Zhaohui Zhang] D;Department of Preventive Medicine, School of public health, Hengyang Medical School, University of South China, Hengyang 421001, Hunan, China
摘要：
Beryllium and its compounds can cause pulmonary interstitial fibrosis through mechanisms that are not yet clear. Long non-coding RNA (lncRNA) is implicated in various diseases. The molecular toxicity of beryllium sulfate (BeSO(4)) was investigated through the RNA-seq analysis of the lncRNA and mRNA whole-transcriptome of BeSO(4)-treated 16HBE cells. A total of 1014 lncRNAs (535 upregulated and 479 downregulated) and 4035 mRNAs (2224 upregulated and 1811 downregulated) were found to be significantly dysregulated (|logFC|≥>2.0, p<0.05) in the BeSO(4)-treated groups when compared with the control group. Five differentially expressed lncRNAs and mRNAs were verified by qRT-PCR. KEGG analysis showed that lncRNA regulates the ECM receiver interaction and PI3K/AKT signaling pathways, etc. In addition, H19:17, lnc-C5orf13-1:1, lnc-CRYAA-17:1, lnc-VSTM5-1:11, and lnc-THSD7A-7:1 may regulate BeSO(4)-induced 16HBE cytotoxicity through ceRNA mechanism. The results of this study will provide some theoretical support for the study of the toxic mechanism of beryllium and its compounds.
作者机构：
[Min, Junxia; Wang, Fudi; Chen, Liyun] Zhejiang Univ, Affiliated Hosp 4, Affiliated Hosp 1,Sch Med, Inst Translat Med,Sch Publ Hlth,State Key Lab Exp, Hangzhou, Peoples R China.;[Wang, Fudi; Chen, Liyun] Univ South China, Affiliated Hosp 1, Sch Publ Hlth, Hengyang Med Sch,Basic Med Sci, Hengyang, Peoples R China.
通讯机构：
[Min, Junxia; Wang, Fudi] T;The Fourth Affiliated Hospital, The First Affiliated Hospital, Institute of Translational Medicine, School of Public Health, State Key Laboratory of Experimental Hematology, Zhejiang University School of Medicine, Hangzhou, China<&wdkj&>The Fourth Affiliated Hospital, The First Affiliated Hospital, Institute of Translational Medicine, School of Public Health, State Key Laboratory of Experimental Hematology, Zhejiang University School of Medicine, Hangzhou, China<&wdkj&>The First Affiliated Hospital, Basic Medical Sciences, School of Public Health, Hengyang Medical School, University of South China, Hengyang, China
摘要：
As an essential micronutrient, copper is required for a wide range of physiological processes in virtually all cell types. Because the accumulation of intracellular copper can induce oxidative stress and perturbing cellular function, copper homeostasis is tightly regulated. Recent studies identified a novel copper-dependent form of cell death called cuproptosis, which is distinct from all other known pathways underlying cell death. Cuproptosis occurs via copper binding to lipoylated enzymes in the tricarboxylic acid (TCA) cycle, which leads to subsequent protein aggregation, proteotoxic stress, and ultimately cell death. Here, we summarize our current knowledge regarding copper metabolism, copper-related disease, the characteristics of cuproptosis, and the mechanisms that regulate cuproptosis. In addition, we discuss the implications of cuproptosis in the pathogenesis of various disease conditions, including Wilson's disease, neurodegenerative diseases, and cancer, and we discuss the therapeutic potential of targeting cuproptosis.
摘要：
Non-alcoholic fatty liver disease (NAFLD), recently re-defined and re-classified as metabolic dysfunction-associated fatty liver disease (MAFLD), has become increasingly prevalent and emerged as a public health problem worldwide. To date, the precise pathogenic mechanisms underpinning MAFLD are not entirely understood, and there is no effective pharmacological therapy for NAFLD/MAFLD. As a newly discovered form of iron-dependent programmed cell death, ferroptosis can be involved in the development and progression of various chronic diseases, but the pathogenic connections and mechanisms that link MAFLD and ferroptosis have not been fully elucidated. The main characteristics of ferroptosis are the accumulation of lipid peroxides and reactive oxygen species. In this brief narrative review, the mechanisms of ferroptosis and its putative pathogenic role in MAFLD are discussed to highlight potential new research directions and ideas for the prevention and treatment of MAFLD.
