Ferroptosis and its modulators: A raising target for cancer and Alzheimer’s disease

Singh, Gourav; Kesharwani, Prashant; Kumar Singh, Gireesh; Kumar, Saroj; Putta, Anjaneyulu; Modi, Gyan

doi:10.1016/j.bmc.2023.117564

Cited by 2 publications

(2 citation statements)

References 207 publications

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“…Clinical research indicates that iron accumulation and oxidative stress are the primary pathological changes in the brains of AD patients. Aβ has been reported to convert intracellular iron to ferrous iron, leading to increased Aβ plaque formation, elevated ferritin expression, and worsening oxidative damage and cognitive impairments ( Lane et al, 2023 ; Singh et al, 2024 ). Moreover, high levels of iron in the brain trigger the production of free radicals and induce oxidative stress.…”

Section: Clinical Diseases Mediated By Ferroptosismentioning

confidence: 99%

Ferroptosis inhibitors: past, present and future

Zhang,

Luo,

Xiang

et al. 2024

Front. Pharmacol.

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Ferroptosis is a non-apoptotic mode of programmed cell death characterized by iron dependence and lipid peroxidation. Since the ferroptosis was proposed, researchers have revealed the mechanisms of its formation and continue to explore effective inhibitors of ferroptosis in disease. Recent studies have shown a correlation between ferroptosis and the pathological mechanisms of neurodegenerative diseases, as well as diseases involving tissue or organ damage. Acting on ferroptosis-related targets may provide new strategies for the treatment of ferroptosis-mediated diseases. This article specifically describes the metabolic pathways of ferroptosis and summarizes the reported mechanisms of action of natural and synthetic small molecule inhibitors of ferroptosis and their efficacy in disease. The paper also describes ferroptosis treatments such as gene therapy, cell therapy, and nanotechnology, and summarises the challenges encountered in the clinical translation of ferroptosis inhibitors. Finally, the relationship between ferroptosis and other modes of cell death is discussed, hopefully paving the way for future drug design and discovery.

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Section: Clinical Diseases Mediated By Ferroptosismentioning

confidence: 99%

Ferroptosis inhibitors: past, present and future

Zhang,

Luo,

Xiang

et al. 2024

Front. Pharmacol.

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“…Mitochondria, the core organelles that control metabolism and produce ROS, are closely related to ferroptosis ( 17 ). Ferroptosis involvement in multiple human diseases has been established, such as gastric cancer, kidney diseases, and Alzheimer’s disease ( 29 - 31 ). These findings suggest that modulating ferroptosis might be potential therapeutic approaches in treating cancer or other diseases.…”

Section: Ferroptosis and Tumorsmentioning

confidence: 99%

Ferroptosis: a promising target for fumarate hydratase-deficient tumor therapeutics literature review

Cheng,

Xia,

Wang

2024

Transl Cancer Res

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Background and Objective This review aims to investigate the ferroptosis mechanism of fumarate hydratase (FH)-related tumors for the purpose of possible treatment of tumors. Ferroptosis is an iron (Fe)-dependent form of regulated cell death caused by lipid peroxidation on the cell membrane. Studies have implicated FH in tumorigenesis. As mutations in the FH gene alter cellular metabolism and increase tumorigenesis risk, particularly in the kidneys. As most tumor cells require higher amounts of ferrous ions (Fe 2+ ) than normal cells, they are more susceptible to ferroptosis. Recent studies have indicated that ferroptosis is inhibited the pathogenesis and progression of FH-deficient tumors by regulating lipid and iron metabolism, glutathione-glutathione peroxidase 4 (GSH-GPX4), nuclear factor-erythroid 2-related factor 2 (NRF2)/heme oxygenase-1 (HO-1) pathways. While the Fe 2+ content is significantly lower in FH-deficient tumor cells, than that in normal cells. It is promising to promote ferroptosis by increasing the concentration of Fe 2+ in cells to achieve the purpose of tumor treatment. Methods In this study, we searched for relevant articles on ferroptosis and FH-deficient tumors using PubMed database. Key Content and Findings FH is a tumor suppressor. A number of basic studies have shown that the loss of FH plays an important role in hereditary leiomyomas and tumors such as renal cell carcinoma, ovarian cancer, and other tumors. This type of tumor cells can through induce ferroptosis, inhibit proliferation, migration and invasion of tumor cells, increase the sensitivity of tumor cells to chemotherapy, and reverse the drug resistance through various molecular mechanisms. At present, the research on ferroptosis in FH-related tumors is still in the basic experimental stage. Conclusions This article reviews the anti-tumor effects and mechanisms of FH and ferroptosis, in order to further explore the medical value of ferroptosis in FH-related tumor therapy.

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Ferroptosis and its modulators: A raising target for cancer and Alzheimer’s disease

Cited by 2 publications

References 207 publications

Ferroptosis inhibitors: past, present and future

Ferroptosis inhibitors: past, present and future

Ferroptosis: a promising target for fumarate hydratase-deficient tumor therapeutics literature review

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