
Non-coding RNA Research, Год журнала: 2025, Номер unknown
Опубликована: Май 1, 2025
Язык: Английский
Non-coding RNA Research, Год журнала: 2025, Номер unknown
Опубликована: Май 1, 2025
Язык: Английский
Cell Death Discovery, Год журнала: 2025, Номер 11(1)
Опубликована: Май 2, 2025
Язык: Английский
Процитировано
0Redox Biology, Год журнала: 2025, Номер unknown, С. 103673 - 103673
Опубликована: Май 1, 2025
Cognitive dysfunction is an essential comorbidity that contributing to the whole disease process of individual chronic obstructive pulmonary (COPD), yet its specific mechanism remains controversial due a lack cellular and molecular evidence. Our clinical data revealed significant reduction in total hippocampal volume patients with COPD, CA1 subfield notably smaller associated lung function. Long-term CS exposure caused hippocampus impairment, leading spatial working memory impairments COPD model mice. triggered ferroptosis vivo vitro. Bioinformatics analysis suggested sestrin2 key ferroptosis-related gene involved cognitive impairment. Sestrin2 protein levels were consistently increased mice CSE treated HT22 cells. knockdown exacerbated enhanced down-regulation synaptophysin PSD95, while overexpression inhibited these damaging processes This neuroprotection dependent on binding heterogeneous nuclear ribonucleoprotein L (HNRNPL). Moreover, DFO ameliorated impairment neurocognitive deficits by correcting CS-induced synaptic proteins alterations vivo. Overall, our study reveals improves adverse changes neurons neurobehavior, providing new insights into mechanisms underlying COPD-related dysfunction.
Язык: Английский
Процитировано
0Biochimica et Biophysica Acta (BBA) - Reviews on Cancer, Год журнала: 2025, Номер 1880(4), С. 189363 - 189363
Опубликована: Май 31, 2025
Язык: Английский
Процитировано
0Non-coding RNA Research, Год журнала: 2025, Номер unknown
Опубликована: Май 1, 2025
Язык: Английский
Процитировано
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