Sestrin2 alleviates cognitive impairment via inhibiting hippocampus ferroptosis in cigarette smoke-induced chronic obstructive pulmonary disease DOI Creative Commons
Dawei Zhang, Mingming Yang,

Meng-Xi Zhou

и другие.

Redox 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

MG53 Deficiency Mediated Skeletal Muscle Dysfunction in Chronic Obstructive Pulmonary Disease Via Impairing Mitochondrial Dynamics DOI
Liwei Liao, Ziwen Zheng, Mingming Deng

и другие.

Опубликована: Янв. 1, 2025

Язык: Английский

Процитировано

0
Additive impact of metabolic syndrome and sarcopenia on all-cause and cause-specific mortality: an analysis of NHANES DOI Creative Commons
Meng Zhang,

Qing-Yue Zeng,

Linli Zhuang

и другие.

Frontiers in Endocrinology, Год журнала: 2025, Номер 15

Опубликована: Фев. 10, 2025

Background Metabolic syndrome (MetS) and sarcopenia (SP) are increasingly significant public health issues in aging societies, sharing common pathophysiological mechanisms being associated with severe consequences. This study investigates the impact of MetS SP on all-cause cause-specific mortality using a longitudinal, nationally representative population-based cohort. Methods The analyzed data from National Health Nutrition Examination Survey (NHANES) conducted between 1999 2018. Mortality were obtained Death Index up to December 2019. Results Among 21,962 participants, 13,517 (61.5%) had neither nor SP(MetS-/SP-), 5,407 (24.6%) only(MetS+/SP-), 2,698 (12.2%) only(MetS-/SP+), 340 (1.5%) both SP(MetS+/SP+). Compared group without SP, groups only, showed increased mortality, adjusted hazard ratios (HR) 1.23 (95% CI: 1.11-1.37), 1.63 1.41-1.89), 1.61 1.33-1.95), respectively. MetS+/SP+ highest overall risk (trend test p<0.0001). For exhibited cardiovascular (HR: 1.89, 95% 1.27-2.81), cardiac 1.25-2.86), respiratory 2.63, 1.29-5.35), diabetes 8.79, 2.62-29.45) compared SP. Conclusion coexistence significantly increases mortality. Individuals either condition may require more vigilant management prevent onset other condition, thereby reducing rates. These findings highlight importance integrated healthcare strategies targeting improve patient outcomes longevity.

Язык: Английский

Процитировано

0
MG53 Deficiency Mediated Skeletal Muscle Dysfunction in Chronic Obstructive Pulmonary Disease via Impairing Mitochondrial Fission DOI Creative Commons
Liwei Liao, Ziwen Zheng, Mingming Deng

и другие.

Redox Biology, Год журнала: 2025, Номер 83, С. 103663 - 103663

Опубликована: Май 3, 2025

Myokine dysregulation and mitochondrial dysfunction are implicated in the pathogenesis of sarcopenia chronic obstructive pulmonary disease. The objective this study is to explore role myokines We identified mitsugumin 53 its clinical correlation through an enzyme-linked immunosorbent assay using plasma samples patients with was confirmed 53-knockout mice. underlying mechanisms were investigated multi-omics sequencing, live-cell imaging, histological molecular experiments. effectiveness safety recombinant treating cigarette smoke-induced muscle evaluated vitro vivo. Plasma levels decreased disease associated skeletal dysfunction. Mitsugumin deficiency exacerbated smoking-induced atrophy. In cells, co-localized mitochondria regulated fission. As a lipid transporter, directly bound mitochondria-specific cardiolipin participated maintaining homeostasis membrane integrity. E3-ligase, deletion triggered BCL2L13-mediated fission upon smoking stimulation. Supplementation significantly alleviated atrophy rescued vital regulator Thus, may be promising therapeutic targets for

Язык: Английский

Процитировано

0
Decoding the Impact of Theabrownin on Skeletal Muscle Function in Gestational Diabetic Offspring: Insights from Integrated Metabolome and Transcriptome Analysis DOI
Rui Liu,

Junsen She,

Xinyuan Li

и другие.

Journal of Agricultural and Food Chemistry, Год журнала: 2025, Номер unknown

Опубликована: Май 6, 2025

Gestational diabetes mellitus (GDM) often leads to long-term metabolic issues, including skeletal muscle dysfunction in the offspring, with traditional managements focusing solely on blood glucose regulation and not addressing structural changes. Theabrownin (TB), a polyphenol derived from Pu-erh tea, has known antioxidant benefits, but its effects function GDM offspring remain unclear. In this study, model was induced mice, their were treated by TB. Transcriptomic metabolomic analyses identified key genes metabolites involved lipid metabolism, oxidative stress, inflammation. TB treatment significantly improved reduced alleviated inflammation of offspring. Key (Fabp3, Acot1, Acot4) (Palmitic acid, Oleic acid) regulated Pathway analysis revealed that mitigates GDM-induced through modulation biosynthesis unsaturated fatty acids. These findings highlight potential theabrownin (TB) as therapeutic agent for improving metabolism. Further investigation is needed elucidate mechanisms evaluate effects.

Язык: Английский

Процитировано

0
Sestrin2 alleviates cognitive impairment via inhibiting hippocampus ferroptosis in cigarette smoke-induced chronic obstructive pulmonary disease DOI Creative Commons
Dawei Zhang, Mingming Yang,

Meng-Xi Zhou

и другие.

Redox 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

0