An overview of ferroptosis in non-alcoholic fatty liver disease DOI Open Access

Shendong Wang,

Zhaojun Liu,

Jiafeng Geng

и другие.

Biomedicine & Pharmacotherapy, Год журнала: 2022, Номер 153, С. 113374 - 113374

Опубликована: Июль 11, 2022

Non-alcoholic fatty liver disease (NAFLD) is a public health problem associated with high mortality and morbidity rates worldwide. Presently, its complex pathophysiology still unclear, there no specific drug to reverse NAFLD. Ferroptosis an iron-dependent non-apoptotic form of cell death characterized by the iron-induced accumulation lipid reactive oxygen species (ROS), which damage nucleic acids, proteins, lipids; generate intracellular oxidative stress; ultimately cause death. Emerging evidence indicates that ferroptosis involved in progression NAFLD, although mechanism action NAFLD poorly understood. Herein, we summarize certain diseases, especially pathogenesis discuss potential therapeutic approaches currently used treat This review also highlights further directions for treatment prevention related diseases.

Язык: Английский

Ferroptosis: A New Regulatory Mechanism in Osteoporosis DOI Creative Commons
Pan Liu, Wenzhao Wang, Zheng Li

и другие.

Oxidative Medicine and Cellular Longevity, Год журнала: 2022, Номер 2022, С. 1 - 10

Опубликована: Янв. 17, 2022

Osteoporosis can be caused by a multitude of factors and is defined decrease in bone density mass the destruction microstructure, resulting increased brittleness. Thus, it systemic disease which patients are prone to fracture. The role ferroptosis pathogenesis osteoporosis has become topic growing interest. In this review, we discuss cell morphology, basic mechanisms ferroptosis, relationship between osteoclasts osteoblasts, as well diabetic osteoporosis, steroid-induced postmenopausal osteoporosis. Emerging biomedical research provided new insights into roles such cellular function, signaling pathways, drug inhibition, gene silencing. pathophysiology mechanism need further studied elucidated broaden our understanding iron metabolism immune regulation. Studies using animal models vivo vitro will help clarify provide ideas for elucidation development technologies drugs treatment future.

Язык: Английский

Процитировано

102

Polyphyllin I induced ferroptosis to suppress the progression of hepatocellular carcinoma through activation of the mitochondrial dysfunction via Nrf2/HO-1/GPX4 axis DOI
Renyi Yang, Wenhui Gao, Zhibing Wang

и другие.

Phytomedicine, Год журнала: 2023, Номер 122, С. 155135 - 155135

Опубликована: Окт. 12, 2023

Язык: Английский

Процитировано

90

Iron, ferroptosis, and ischemic stroke DOI Open Access
Jun Guo, Qing‐zhang Tuo, Peng Lei

и другие.

Journal of Neurochemistry, Год журнала: 2023, Номер 165(4), С. 487 - 520

Опубликована: Март 13, 2023

Abstract Over 30 million people suffer from the consequences of ischemic stroke. The precise molecular mechanism neuronal damage during stroke remains unclear; therefore, effective treatment post‐ischemic a critical challenge. Recently, iron has emerged as crucial factor in post‐reperfusion injuries, participating cell peroxidation, excitotoxicity, and distinctive death pathway, namely, ferroptosis. Since is tightly regulated brain important for functions, imbalance its metabolism, including overload deficiency, been shown to impact outcomes. This review summarizes current understanding pathological events associated with discusses relevant drug development. image

Язык: Английский

Процитировано

86

Targeting epigenetic and posttranslational modifications regulating ferroptosis for the treatment of diseases DOI Creative Commons
Yumin Wang, Jing Hu, Shuang Wu

и другие.

Signal Transduction and Targeted Therapy, Год журнала: 2023, Номер 8(1)

Опубликована: Дек. 10, 2023

Abstract Ferroptosis, a unique modality of cell death with mechanistic and morphological differences from other modes, plays pivotal role in regulating tumorigenesis offers new opportunity for modulating anticancer drug resistance. Aberrant epigenetic modifications posttranslational (PTMs) promote resistance, cancer progression, metastasis. Accumulating studies indicate that can transcriptionally translationally determine vulnerability to ferroptosis functions as driver nervous system diseases (NSDs), cardiovascular (CVDs), liver diseases, lung kidney diseases. In this review, we first summarize the core molecular mechanisms ferroptosis. Then, roles processes, including histone PTMs, DNA methylation, noncoding RNA regulation such phosphorylation, ubiquitination, SUMOylation, acetylation, ADP-ribosylation, are concisely discussed. The PTMs genesis cancers, NSD, CVDs, well application PTM modulators therapy these then discussed detail. Elucidating mediated by will facilitate development promising combination therapeutic regimens containing or PTM-targeting agents inducers be used overcome chemotherapeutic resistance could prevent addition, highlight potential approaches chemoresistance halt

Язык: Английский

Процитировано

84

An overview of ferroptosis in non-alcoholic fatty liver disease DOI Open Access

Shendong Wang,

Zhaojun Liu,

Jiafeng Geng

и другие.

Biomedicine & Pharmacotherapy, Год журнала: 2022, Номер 153, С. 113374 - 113374

Опубликована: Июль 11, 2022

Non-alcoholic fatty liver disease (NAFLD) is a public health problem associated with high mortality and morbidity rates worldwide. Presently, its complex pathophysiology still unclear, there no specific drug to reverse NAFLD. Ferroptosis an iron-dependent non-apoptotic form of cell death characterized by the iron-induced accumulation lipid reactive oxygen species (ROS), which damage nucleic acids, proteins, lipids; generate intracellular oxidative stress; ultimately cause death. Emerging evidence indicates that ferroptosis involved in progression NAFLD, although mechanism action NAFLD poorly understood. Herein, we summarize certain diseases, especially pathogenesis discuss potential therapeutic approaches currently used treat This review also highlights further directions for treatment prevention related diseases.

Язык: Английский

Процитировано

74