Nrf2/UBE3B protects against acute lung injury by inhibiting ferritinophagy through the ubiquitination of NCOA4 DOI Creative Commons
Yanjun Wang, Hui Dong, Yunfan Gu

и другие.

Research Square (Research Square), Год журнала: 2024, Номер unknown

Опубликована: Окт. 14, 2024

Abstract Iron overload and ferroptosis are associated with intestinal ischemia reperfusion (II/R)-induced acute lung injury (ALI). However, the mechanisms underlying regulation of iron homeostasis remain unclear. Nrf2 regulates cellular homeostasis; however, its impact on ALI pathology mechanism action requires further investigation. Ubiquitin ligase E3B (UBE3B) plays a critical role in proteasome pathway, which is essential for protein turnover ubiquitin-mediated signaling. A recent study found that UBE3B oxidative stress; it remains unknown whether related to Nrf2. Furthermore, exact largely uncharacterized. In present study, immunohistochemical analysis expression type II alveolar epithelial cells (AECII) was conducted be increased II/R-ALI. Western blot indicated hyperactivation may alleviate stress, thereby protecting against ALI. Moreover, involved metabolism dysfunction ferroptosis. deficiency enhanced process nuclear receptor coactivator 4 (NCOA4)-mediated ferritinophagy ferrous ion content, whereas overexpression reversed harmful effects knockdown AECⅡ, promote AECⅡ This highlights Nrf2/UBE3B/NCOA4 axis II/R-ALI pathogenesis, suggesting activation promising strategy treatment.

Язык: Английский

Nuclear receptor coactive 4-mediated ferritinophagy: a key role of heavy metals toxicity DOI

Wan-Xue Xu,

Wen Xue, Yupeng Fu

и другие.

Archives of Toxicology, Год журнала: 2025, Номер unknown

Опубликована: Фев. 10, 2025

Язык: Английский

Процитировано

2
Zearalenone induces liver injury in mice through ferroptosis pathway DOI

Lige Bao,

Yongze Huang,

Fuhua Gu

и другие.

The Science of The Total Environment, Год журнала: 2024, Номер 952, С. 175875 - 175875

Опубликована: Авг. 30, 2024

Язык: Английский

Процитировано

8
Hesperidin Alleviates Hepatic Injury Caused by Deoxynivalenol Exposure through Activation of mTOR and AKT/GSK3β/TFEB Pathways DOI

Xin Wang,

Hao Chen, Junze Jiang

и другие.

Journal of Agricultural and Food Chemistry, Год журнала: 2024, Номер 72(25), С. 14349 - 14363

Опубликована: Июнь 13, 2024

Deoxynivalenol (DON) is a common agricultural mycotoxin that chemically stable and not easily removed from cereal foods. When organisms consume food made contaminated crops, it can be hazardous to their health. Numerous studies in recent years have found hesperidin (HDN) has hepatoprotective effects on wide range of toxins. However, few scholars explored the potential HDN attenuating DON-induced liver injury. In this study, we established low-dose DON exposure model intervened with three doses HDN, acting male C57 BL/6 mice AML12 cells, which served as vivo vitro models, respectively, investigate protective mechanism against exposure-induced The results suggested disrupted hepatic autophagic fluxes, thereby impairing structure function, significantly attenuated these changes. Further revealed alleviated excessive autophagy through mTOR pathway lysosomal dysfunction AKT/GSK3β/TFEB pathway. Overall, our study could ameliorate flux disorders via pathway, reducing

Язык: Английский

Процитировано

7
18beta-glycyrrhetinic acid alleviates deoxynivalenol-induced hepatotoxicity by inhibiting GPX4-dependent ferroptosis DOI

Chenchen Song,

Wei Wang,

Yu Hua

и другие.

Toxicon, Год журнала: 2025, Номер unknown, С. 108228 - 108228

Опубликована: Янв. 1, 2025

Язык: Английский

Процитировано

1
Ferritinophagy: multifaceted roles and potential therapeutic strategies in liver diseases DOI Creative Commons

Kejia Wu,

Wei Zhao,

Zeyu Hou

и другие.

Frontiers in Cell and Developmental Biology, Год журнала: 2025, Номер 13

Опубликована: Фев. 25, 2025

Ferritinophagy, the selective autophagic degradation of ferritin to release iron, is emerging as a critical regulator iron homeostasis and key player in pathogenesis various liver diseases. This review comprehensively examines mechanisms, regulation, multifaceted roles ferritinophagy health disease. Ferritinophagy intricately regulated by several factors, including Nuclear Receptor Coactivator 4 (NCOA4), Iron regulatory proteins signaling pathways such mTOR AMPK. These mechanisms ensure proper utilization prevent overload, which can induce oxidative stress ferroptosis. In diseases, exhibits dual roles. fibrosis, promoting hepatic stellate cells (HSCs) cell senescence reduce fibrosis progression. However, non-alcoholic fatty disease (NAFLD), chronic may exacerbate injury through overload stress. hepatocellular carcinoma (HCC), be harnessed novel therapeutic strategy inducing ferroptosis cancer cells. Additionally, implicated drug-induced sepsis-associated damage, highlighting its broad impact on pathology. also explores crosstalk between other autophagy pathways, mitophagy lipophagy, collectively influence cellular Understanding these interactions essential for developing comprehensive strategies targeting multiple pathways. summary, complex dynamic process with significant implications provides an in-depth analysis ferritinophagy's potential target, emphasizing need further research elucidate role

Язык: Английский

Процитировано

1
Naringenin alleviates liver fibrosis by triggering autophagy-dependent ferroptosis in hepatic stellate cells DOI Creative Commons
Ting Yu,

Xuejia Lu,

Liang Yan

и другие.

Heliyon, Год журнала: 2024, Номер 10(7), С. e28865 - e28865

Опубликована: Март 29, 2024

Inhibition of activated hepatic stellate cells (HSCs) is a promising approach for treating liver fibrosis, and the ferroptosis has emerged as pivotal mechanism to achieve this inhibition. The effects naringenin, flavonoid with anti-inflammatory properties, have not been thoroughly examined in fibrosis. Therefore, we used cholestasis model study effect naringenin on Our findings demonstrated significant exacerbation tissue damage fibrosis mice subjected bile duct ligation (BDL), accompanied by substantial upregulation fibrogenesis-related gene expression. Notably, administration markedly alleviated injury these mice. Furthermore, exhibited inhibitory activation HSCs, concurrently inducing ferroptosis. Importantly, significantly increased autophagic activity HSCs. This was counteracted co-administration autophagy inhibitor 3-MA, leading notable reduction naringenin-induced HSC In BDL mice, mitigating suggesting potential correlation These results provide novel insights into molecular mechanisms highlight autophagy-dependent therapeutic strategy

Язык: Английский

Процитировано

6
Cu2O nanoparticles with morphology-dependent peroxidase mimic activity: a novel colorimetric biosensor for deoxynivalenol detection DOI
Xiaodong Zhu,

BoBo Zhang,

Junhao Wang

и другие.

Microchimica Acta, Год журнала: 2024, Номер 191(10)

Опубликована: Сен. 10, 2024

Язык: Английский

Процитировано

5
CYP2E1 mediated deoxynivalenol-induced hepatocyte toxicity by regulating ferroptosis DOI
Qigui Mo,

Chenchen Song,

Yu Hua

и другие.

Toxicology, Год журнала: 2024, Номер 508, С. 153923 - 153923

Опубликована: Авг. 13, 2024

Язык: Английский

Процитировано

4
Low-dose deoxynivalenol exposure triggers hepatic excessive ferritinophagy and mitophagy mitigated by hesperidin modulated O-GlcNAcylation DOI
Hao Chen,

Xintong Zhou,

Jun Ma

и другие.

Journal of Hazardous Materials, Год журнала: 2024, Номер 480, С. 135952 - 135952

Опубликована: Сен. 24, 2024

Язык: Английский

Процитировано

3
Targeting Ferroptosis and Ferritinophagy Improves Tooth Extraction Socket Healing in Type 2 Diabetes Mellitus Via Human Bone Marrow Mesenchymal Stem Cells Modulation DOI
Yifeng Bian, Jianfeng Li, Fan Xu

и другие.

Опубликована: Янв. 1, 2025

Язык: Английский

Процитировано

0