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

Cell Communication and Signaling, Journal Year: 2024, Volume and Issue: 22(1)

Published: Oct. 11, 2024

Disulfidptosis is a novel discovered form of programmed cell death (PCD) that diverges from apoptosis, necroptosis, ferroptosis, and cuproptosis, stemming disulfide stress-induced cytoskeletal collapse. In cancer cells exhibiting heightened expression the solute carrier family 7 member 11 (SLC7A11), excessive cystine importation reduction will deplete nicotinamide adenine dinucleotide phosphate (NADPH) under glucose deprivation, followed by an increase in intracellular stress aberrant bond formation within actin networks, ultimately culminating collapse disulfidptosis. involves crucial physiological processes eukaryotic cells, such as uptake, NADPH metabolism, dynamics. The Rac1-WRC pathway-mediated polymerization also implicated this due to its contribution formation. However, precise mechanisms underlying disulfidptosis role tumors are not well understood. This probably multifaceted functionalities SLC7A11 complexities downstream pathways driving review describes critical roles summarizes recent research advancements potential Moreover, less-studied aspects newly process highlighted stimulate further investigations field.

Language: Английский

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The impact of bisphenol A on gill health: A focus on mitochondrial dysfunction induced disorders of energy metabolism and apoptosis in Meretrix petechialis

Aquatic Toxicology, Journal Year: 2025, Volume and Issue: 279, P. 107259 - 107259

Published: Jan. 27, 2025

Language: Английский

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Disulfidptosis: a new target for central nervous system disease therapy

Frontiers in Neuroscience, Journal Year: 2025, Volume and Issue: 19

Published: March 5, 2025

Disulfidptosis is a pathologic process that occurs under conditions of NADPH deficiency and excess disulfide bonds in cells express high levels SLC7A11. This caused by glucose deprivation-induced stress was first described cancer researchers. Oxidative hypothesized mechanism underlying diseases the central nervous system (CNS), specific type oxidative stress. Proteins linked to disulfidptosis metabolic pathways involved are significantly associated with CNS (neurodegenerative disease, neurogliomas ischemic stroke). However, responsible for this correlation remains unknown. review provides comprehensive overview current knowledge regarding origin elements, genetic factors, signaling proteins pathogenesis disulfidptosis. It demonstrates disruption thiometabolism play critical roles diseases, which potential role We also summarize disulfidptosis-related drugs highlight therapeutic strategies treating diseases. Additionally, paper suggests testable hypothesis might be promising target

Language: Английский

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Dock1 functions in Schwann cells to regulate development, maintenance, and repair

The Journal of Cell Biology, Journal Year: 2025, Volume and Issue: 224(5)

Published: Feb. 11, 2025

Schwann cells, the myelinating glia of peripheral nervous system (PNS), are critical for myelin development, maintenance, and repair. Rac1 is a known regulator radial sorting, key step in developmental myelination. Previously, zebrafish, we showed that loss Dock1, Rac1-specific guanine nucleotide exchange factor, resulted delayed myelination during development. Here, demonstrate Dock1 necessary maintenance remyelination after injury adult zebrafish. Furthermore, performs an evolutionarily conserved role mice, functioning cell autonomously cells to regulate repair myelin. Pharmacological genetic manipulation larval along with analysis active levels developing mutant mouse nerves, revealed interaction between these two proteins. We propose interplay signaling required establish, maintain, facilitate within PNS.

Language: Английский

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Inhibition of Rac1 attenuated propofol-induced neurotoxicity in the hippocampal dentate gyrus in developing mice

Research Square (Research Square), Journal Year: 2025, Volume and Issue: unknown

Published: April 10, 2025

Accumulating evidence from animals has shown that multiple exposures to general anesthetics during brain development may cause extensive neuronal apoptosis and long-term memory impairments. However, the underlying mechanism is still poorly understood. In present study, C57BL/6 mice were administered propofol at postnatal days 19–21. We found exposure significantly increased in mouse hippocampal dentate gyrus, as evidenced by cleaved caspase-3 (c-c3) immunofluorescence. Additionally, activation expression of Ras-related C3 botulinum toxin substrate 1 (Rac1) western blotting. Modulating Rac1, either through inhibition or overexpression, was mitigate exacerbate propofol-induced apoptosis, respectively. further demonstrated decreased antiapoptotic protein phosphorylated serine/threonine kinase Akt via Rac1. The results open field morris water maze tests revealed silencing Rac1 alleviated cognitive dysfunction. Our findings induced dysfunction gyrus regulating

Language: Английский

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Alkaloids from the medicinal plant Incarvillea sinensis: Molecular diversity, synthesis, pharmacological properties and mechanism of action

Fitoterapia, Journal Year: 2025, Volume and Issue: 183, P. 106548 - 106548

Published: April 15, 2025

Language: Английский

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RAC1 serves as a prognostic factor and correlated with immune infiltration in liver hepatocellular carcinoma

Journal of Cancer Research and Clinical Oncology, Journal Year: 2024, Volume and Issue: 150(9)

Published: Sept. 12, 2024

Language: Английский

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