Disulfidptosis: A new type of cell death

Xiao, Fei; Li, Hui-Li; Yang, Bei; Che, Hao; Xu, Fei; Li, Gang; Zhou, Cheng-Hui; Wang, Sheng

doi:10.1007/s10495-024-01989-8

Apoptosis

2024

DOI: 10.1007/s10495-024-01989-8

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Disulfidptosis: A new type of cell death

Fei Xiao,

Hui-Li Li,

Bei Yang

et al.

Abstract: Disulfidptosis is a novel form of cell death that is distinguishable from established programmed cell death pathways such as apoptosis, pyroptosis, autophagy, ferroptosis, and oxeiptosis. This process is characterized by the rapid depletion of nicotinamide adenine dinucleotide phosphate (NADPH) in cells and high expression of solute carrier family 7 member 11 (SLC7A11) during glucose starvation, resulting in abnormal cystine accumulation, which subsequently induces andabnormal disulfide bond formation in actin… Show more

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2024

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Cited by 3 publications

References 140 publications

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Disulfidptosis: a novel cell death modality induced by actin cytoskeleton collapse and a promising target for cancer therapeutics

Li,

Song,

Wei

et al. 2024

Cell Commun Signal

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Disulfidptosis: a novel cell death modality induced by actin cytoskeleton collapse and a promising target for cancer therapeutics

Li,

Song,

Wei

et al. 2024

Cell Commun Signal

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Interplay of cell death pathways and immune responses in ischemic stroke: insights into novel biomarkers

Daneshpour,

Shaka,

Rezaei

2024

Reviews in the Neurosciences

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Stroke is a severe neurological disease and a major worldwide issue, mostly manifesting as ischemic stroke (IS). In order to create effective treatments for IS, it is imperative to fully understand the underlying pathologies, as the existing therapeutic choices are inadequate. Recent investigations have shown the complex relationships between several programmed cell death (PCD) pathways, including necroptosis, ferroptosis, and pyroptosis, and their correlation with immune responses during IS. However, this relationship is still unclear. To address this gap, this review study explored the cellular interactions in the immune microenvironment of IS. Then, to validate prior findings and uncover biomarkers, the study investigated bioinformatics studies. Several pathways, including nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), Toll-like receptor 4 (TLR4), and receptor-interacting protein kinase (RIPK), were involved in PCD-immune interactions. The bioinformatics studies reported key biomarkers such as glutathione peroxidase 4 (GPX4), NOD-like receptor family pyrin domain containing 3 (NLRP3), gasdermin D (GSDMD), and TLR4, which have important implications in ferroptosis, cuproptosis, pyroptosis, and necroptosis respectively. These biomarkers were associated with PCD mechanisms such as oxidative stress and inflammatory reactions. The immune infiltration analysis consistently revealed a significant correlation between PCD pathways and detrimental immune cells, such as neutrophils and γδ T cells. Conversely, M2 macrophages and T helper cells showed protective effects. In conclusion, considering the intricate network of interactions between immune responses and PCD pathways, this study emphasized the necessity of a paradigm shift in therapeutic approaches to address the injuries that are related to this complex network.

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Targeting Disulfidptosis with Potentially Bioactive Natural Products in Metabolic Cancer Therapy

Li,

Xu,

Yan

et al. 2024

Metabolites

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Background: Metabolic cancers are defined by metabolic reprogramming. Although this reprograming drives rapid tumour growth and invasion, it also reveals specific metabolic vulnerabilities that can be therapeutically exploited in cancer therapy. A novel form of programmed cell death, known as disulfidptosis, was identified last year; tumour cells with high SLC7A11 expression undergo disulfidptosis when deprived of glucose. Natural products have attracted increasing attention and have shown potential to treat metabolic cancers through diverse mechanisms. Methods: We systematically searched electronic databases involving PubMed, Web of Science, Gooale Scholar. To ensue comprehensive exploration, keywords including metabolic reprogramming, metabolic cancer, disulfidptosis, natural products and some other words were employed. Results: In this review, we focus on the shared characteristics and metabolic vulnerabilities of metabolic cancers. Additionally, we discuss the molecular mechanisms underlying disulfidptosis and highlight key regulatory genes. Furthermore, we predict bioactive natural products that target disulfidptosis-related genes, offering new perspectives for anticancer strategies through the modulation of disulfidptosis. Conclusions: By summarizing current research progress, this review mainly analyzed the potential mechanisms of natural products in the treatment of metabolic cancer.

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Disulfidptosis: A new type of cell death

Cited by 3 publications

References 140 publications

Disulfidptosis: a novel cell death modality induced by actin cytoskeleton collapse and a promising target for cancer therapeutics

Disulfidptosis: a novel cell death modality induced by actin cytoskeleton collapse and a promising target for cancer therapeutics

Interplay of cell death pathways and immune responses in ischemic stroke: insights into novel biomarkers

Targeting Disulfidptosis with Potentially Bioactive Natural Products in Metabolic Cancer Therapy

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