Article
Pharmacology & Pharmacy
Milica Kosic, Verica Paunovic, Biljana Ristic, Aleksandar Mircic, Mihajlo Bosnjak, Danijela Stevanovic, Tamara Kravic-Stevovic, Vladimir Trajkovic, Ljubica Harhaji-Trajkovic
Summary: The study showed that 3-methyladenine (3MA) can prevent cancer cell death induced by energy stress through autophagy-independent mechanisms, possibly involving JNK suppression and decrease of oxidative stress. It highlights the need for caution when using 3MA as an autophagy inhibitor.
JOURNAL OF PHARMACOLOGICAL SCIENCES
(2021)
Review
Cell Biology
Xin Chen, Jingbo Li, Rui Kang, Daniel J. Klionsky, Daolin Tang
Summary: Ferroptosis is an iron-dependent, non-apoptotic form of regulated cell death caused by lipid peroxidation. Lipoxygenase is the main promoter of ferroptosis, while GPX4 is the central repressor of this process.
Article
Biochemistry & Molecular Biology
Fangquan Chen, Xiutao Cai, Rui Kang, Jiao Liu, Daolin Tang
Summary: Autophagy determines cell fate in response to environmental stresses and its dependence in cell death signals and mechanisms are still unclear. The discovery of autophagy-dependent ferroptosis provides insights into the relationship between aberrant degradation pathways and excessive lipid peroxidation in driving regulated cell death.
ANTIOXIDANTS & REDOX SIGNALING
(2023)
Article
Cell Biology
Konstantin G. Lyamzaev, Alisa A. Panteleeva, Ruben A. Simonyan, Armine V. Avetisyan, Boris V. Chernyak
Summary: Ferroptosis induced by erastin and butionine sulfoximine can be prevented by the mitochondria-targeted antioxidants SkQ1 and MitoTEMPO. This prevention is associated with the inhibition of mitochondrial lipid peroxidation, which occurs before cell death. Methylene blue, a redox agent that inhibits reactive oxygen species (ROS) production in complex I of the mitochondrial electron transport chain, also inhibits ferroptosis and mitochondrial lipid peroxidation. We propose that ROS generated in complex I promote mitochondrial lipid peroxidation and ferroptosis.
Article
Biochemistry & Molecular Biology
Wuyang Lv, Lei Liang, Dongyang Liu, Cuicui Li, Liao Jia, Yingyu Jin
Summary: This study investigated the role of AQP1 in ferroptosis, macrophage polarization, mitochondrial dysfunction, and impaired autophagy of LPS-stimulated RAW264.7 cells. The results showed that AQP1 promotes ferroptosis, M1 polarization, mitochondrial dysfunction, and autophagy impairment by inhibiting the expression of P53 in LPS-stimulated RAW264.7 cells. AQP1 or P53 may be considered as crucial determiners that regulate the biological behavior of RAW264.7 cells stimulated by LPS.
DNA AND CELL BIOLOGY
(2023)
Review
Immunology
Xu-Dong Zhang, Zhong-Yuan Liu, Mao-Sen Wang, Yu-Xiang Guo, Xiang-Kun Wang, Kai Luo, Shuai Huang, Ren-Feng Li
Summary: Regulation of cell mortality for disease treatment has been a focus of research, with the iron-dependent regulated cell death called Ferroptosis being extensively studied. Studies have shown that regulation of ferroptosis brings new treatment strategies for various diseases. Genes involved in iron and lipid metabolism can regulate ferroptosis by controlling iron overload and lipid peroxidation. Glutathione (GSH), the body's primary non-enzymatic antioxidant, also plays a crucial role in combating lipid peroxidation by assisting glutathione peroxidase 4 (GPX4). This review summarizes recent research on the mechanism of ferroptosis and comprehensively analyzes the regulation of ferroptosis through iron and lipid metabolism, as well as the metabolism of GPX4 and GSH.
FRONTIERS IN IMMUNOLOGY
(2023)
Article
Cell Biology
Jingbo Li, Jiao Liu, Yinghua Xu, Runliu Wu, Xin Chen, Xinxin Song, Herbert Zeh, Rui Kang, Daniel J. Klionsky, Xiaoyan Wang, Daolin Tang
Summary: Autophagy plays a complex role in cellular stress and can either promote survival or trigger death. Recent evidence suggests that the molecular machinery of autophagy facilitates ferroptosis, a regulated cell death process. The study found tumor heterogeneity in autophagy-dependent ferroptosis, showing different biological behaviors in terms of cell death dynamics.
Review
Immunology
Xiaodi Lv, Weifeng Tang, Jingjing Qin, Wenqian Wang, Jingcheng Dong, Ying Wei
Summary: Autophagy is a cellular process that degrades molecules and organelles via the lysosomal pathway, while ferroptosis is an oxidative stress-dependent cell death associated with iron accumulation and lipid peroxidation. The crosslinks between autophagy and ferroptosis are closely related to the treatment of various diseases.
FRONTIERS IN IMMUNOLOGY
(2023)
Review
Endocrinology & Metabolism
Jiahui He, Zhangwang Li, Panpan Xia, Ao Shi, Xinxi FuChen, Jing Zhang, Peng Yu
Summary: This review systematically explores the roles and regulatory mechanisms of ferroptosis and ferritinophagy in diabetes complications and highlights their potential therapeutic value. However, further research is needed to fully understand their molecular mechanisms and pathophysiological processes involved.
MOLECULAR METABOLISM
(2022)
Article
Endocrinology & Metabolism
Ruiqi Ma, Lu Gan, Jie Guo, Zhiyu Peng, Jihong Wu, Andrew R. Harrison, Jiang Qian
Summary: This study reveals that Graves' orbitopathy (GO) orbital fibroblasts (OFs) exhibit stronger resistance to ferroptosis compared to control OFs. GO OFs undergo a glycolytic shift. Inhibition of glycolysis enhances ferroptosis sensitivity in GO OFs. Overexpression of IGF1R contributes to the glycolytic shift in GO OFs.
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
(2022)
Article
Cell Biology
Yanchun Li, Xin Wang, Zhihui Huang, Yi Zhou, Jun Xia, Wanye Hu, Xu Wang, Jing Du, Xiangmin Tong, Ying Wang
Summary: CISD3 plays a crucial regulatory role in cancer progression and ferroptosis, with its overexpression associated with poorer survival rates, while its depletion accelerates ferroptotic cell death. Depletion of CISD3 leads to metabolic reprogramming towards glutaminolysis, which is essential for mitochondrial oxidative phosphorylation.
CELL DEATH & DISEASE
(2021)
Article
Materials Science, Multidisciplinary
Kangqiang Qiu, Aditya Yadav, Zhiqi Tian, Ziyuan Guo, Donglu Shi, Chayan K. Nandi, Jiajie Diao
Summary: In this study, biocompatible protein-modified noble-metal nanoclusters were used to image lysosomes under structured illumination microscopy. The nanoclusters exhibited excellent performance in pH fluctuation resistance and antiphotobleaching, allowing for the observation of lysosomal events and the interplay between lysosomes and mitochondria. This research opens up new possibilities for long-term bioimaging with nanoclusters.
ACS MATERIALS LETTERS
(2022)
Article
Biology
Laure Perrin-Cocon, Pierre-Olivier Vidalain, Clemence Jacquemin, Anne Aublin-Gex, Keedrian Olmstead, Baptiste Panthu, Gilles Jeans Philippe Rautureau, Patrice Andre, Piotr Nyczka, Marc-Thorsten Huett, Nivea Amoedo, Rodrigue Rossignol, Fabian Volker Filipp, Vincent Lotteau, Olivier Diaz
Summary: During the transformation into hepatocellular carcinoma, the replacement of GCK by HK2 is associated with poor prognosis for patient survival. Knocking out HK2 and expressing GCK in Huh7 cell line rewired central carbon metabolism, stimulated mitochondrial respiration, and reactivated innate immune responses, showing that consequences of the HK switch extend beyond metabolic reprogramming.
COMMUNICATIONS BIOLOGY
(2021)
Review
Multidisciplinary Sciences
Yuyan Xie, Yang Zhou, Jiale Wang, Lijuan Du, Yuanyuan Ren, Fang Liu
Summary: Ferroptosis, a new form of cell death, is closely related to autophagy, and both play important roles in tumor progression, treatment, and drug resistance.
Review
Medicine, Research & Experimental
Tian-Liang Ma, Jing-Xian Chen, Peng Zhu, Chao-Bin Zhang, Yong Zhou, Jia-Xi Duan
Summary: Ferroptosis is an iron-dependent regulatory necrosis characterized by the accumulation of iron-dependent lipid peroxides in the plasma membrane and subsequent oxidative damage. It is mainly related to iron toxicity, lipid peroxidation, and mitochondrial dysfunction. Understanding the specific mechanism of ferroptosis and exploring strategies for its regulation have significant clinical implications.