Results 1 to 10 of about 2,022 (185)
The mystery about the mechanistic basis of disulfidptosis has recently been unraveled and shows promise as an effective treatment modality for triggering cancer cell death.
Furong Zeng, Guangtong Deng, Yating Dian
exaly +6 more sources
Disruption of disulfide homeostasis during biological processes can have fatal consequences. Excess disulfides induce cell death in a novel manner, termed as “disulfidptosis.” However, the specific mechanism of disulfidptosis has not yet been elucidated.
Ning Li, Hailin Tang, Yutian Zou
exaly +3 more sources
Recent studies have found that disulfidptosis occurs in cells under glucose starvation. The role of this programmed death method in gastric cancer remains to be explored.
Wenxue Wu, Zhiqing Chen
exaly +4 more sources
Disulfidptosis: Mechanisms, evidence boundaries, and translational opportunities [PDF]
Disulfidptosis has rapidly emerged as a regulated cell death mechanism linked to cystine stress, aberrant disulfide accumulation, and collapse of the actin cytoskeleton, particularly in contexts shaped by high SLC7A11 activity and impaired NADPH ...
Rongqing Li +3 more
doaj +3 more sources
Disulfidptosis refers to a specific programmed cell death process characterized by the accumulation of disulfides. It has recently been reported in several cancers. However, the impact of disulfidptosis-related long non-coding RNAs (lncRNAs) on malignant
Dong-liang Lin +2 more
exaly +4 more sources
Disulfidptosis- and Ferroptosis-Related Gene Signatures in Rheumatoid Arthritis: Association Analysis and Diagnostic Model Construction. [PDF]
ABSTRACT Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by persistent synovial inflammation and progressive joint damage. Although ferroptosis has been implicated in RA progression, the role of disulfidptosis and its interaction with ferroptosis remains unclear.
Wang TT +10 more
europepmc +2 more sources
Age‐Related Lamin B1 Deficiency Activates SLC7A11‐Dependent Disulfidptosis to Impair Osteogenesis via Intercepting Mitochondrial Fission [PDF]
This study reveals that age‐related LMNB1 deficiency in mesenchymal stem cells epigenetically upregulates SLC7A11, triggering actin disulfidptosis and mitochondrial dysfunction. This cascade impairs bone formation in senile osteoporosis. Furthermore, researchers identified the FDA‐approved drug naldemedine as a targeted SLC7A11 inhibitor to reverse ...
Yu W +12 more
europepmc +2 more sources
YTHDC1 Orchestrates Glucose and Glutamate Rewiring to Overcome Lethal Metabolic Stress in Triple-Negative Breast Cancer. [PDF]
Lai et al. find that m6A reader YTHDC1 is specifically overexpressed in triple‐negative breast cancer (TNBC) and orchestrates glucose and glutamine metabolism in an m6A‐dependent manner to confer robust adaptability to lethal metabolic stress. Leveraging YTHDC1 knockdown‐induced metabolic vulnerability, an ATF4 mRNA‐targeted nanotherapy is developed to
Lai ZH +12 more
europepmc +2 more sources
Tumor Microenvironment-Responsive Nanoreactor Induces Disulfidptosis in Pancreatic Cancer via Metabolic Interference and Redox Catalysis. [PDF]
Schematic illustration of a tumor microenvironment‐responsive nanoreactor for imaging‐guided induction of disulfidptosis in pancreatic cancer via metabolic interference and redox catalysis. (A) Stepwise fabrication of Pht@HMnO2‐HA, including MnO2 growth on a SiO2 template, template removal to form hollow mesoporous MnO2, Pht loading, and subsequent ...
Fu R +10 more
europepmc +2 more sources
Background: Emerging evidence suggests that cell deaths are involved in tumorigenesis and progression, which may be treated as a novel direction of cancers. Recently, a novel type of programmed cell death, disulfidptosis, was discovered.
Linhui Wang, Baohua Zhu, Wenqiang Liu
exaly +3 more sources

