Ageing Research Reviews, Год журнала: 2024, Номер 103, С. 102600 - 102600
Опубликована: Ноя. 30, 2024
Язык: Английский
Ageing Research Reviews, Год журнала: 2024, Номер 103, С. 102600 - 102600
Опубликована: Ноя. 30, 2024
Язык: Английский
Frontiers in Immunology, Год журнала: 2025, Номер 15
Опубликована: Янв. 23, 2025
Background The involvement of mitochondrial and programmed cell death (mtPCD)–related genes in the pathogenesis pre-eclampsia (PE) remains inadequately characterized. Methods This study explores role mtPCD PE through bioinformatics experimental approaches. Differentially expressed were identified as potential biomarkers from GSE10588 GSE98224 datasets subsequently validated. Hub determined using support vector machine, least absolute shrinkage selection operator, Boruta based on consistent expression profiles. Their performance was assessed nomogram artificial neural network models. Biomarkers subjected to localization, functional annotation, regulatory analysis, drug prediction. Clinical validation conducted via real-time quantitative polymerase chain reaction (RT-qPCR), immunofluorescence, Western blot. Results Four [solute carrier family 25 member 5 ( SLC25A5 ), acyl-CoA synthetase 2 ACSF2 fission factor MFF phorbol-12-myristate-13-acetate–induced protein 1 PMAIP1 )] distinguishing normal controls. Functional analysis indicated their various biological pathways. Immune revealed associations between immune activity. A informed by biomarker database predictions, which KCNQ1OT1 modulates hsa-miR-200b-3p. Drug including clodronic acid, also proposed. Immunofluorescence, RT-qPCR, blot confirmed reduced SLC25A5, , PE, whereas significantly upregulated. Conclusion These four mtPCD-related may play a pivotal pathogenesis, offering new perspectives disease’s diagnostic mechanistic
Язык: Английский
Процитировано
0Biochimica et Biophysica Acta (BBA) - Molecular Cell Research, Год журнала: 2025, Номер unknown, С. 119911 - 119911
Опубликована: Янв. 1, 2025
Язык: Английский
Процитировано
0Frontiers in Cell and Developmental Biology, Год журнала: 2025, Номер 13
Опубликована: Фев. 26, 2025
Enhanced Drp1 activity mediates excessive mitochondrial fission, contributing to the onset and progression of various chronic diseases, including neurodegenerative, cardiovascular, metabolic disorders. Studies indicate that exercise mitigates dysfunction by modulating Drp1-related signaling targets, thereby inhibiting reducing fission. This, in turn, enhances function cellular metabolism. This review synthesizes current understanding structure activation mechanisms, analyzes effects interventions on Drp1-mediated fission different disease models improve common conditions. research deepens our insight into specific mechanisms Drp1-induced pathogenesis, offering new theoretical support practical guidance for as a non-pharmacological intervention strategy.
Язык: Английский
Процитировано
0Chemico-Biological Interactions, Год журнала: 2025, Номер unknown, С. 111492 - 111492
Опубликована: Март 1, 2025
Язык: Английский
Процитировано
0Ageing Research Reviews, Год журнала: 2024, Номер 103, С. 102600 - 102600
Опубликована: Ноя. 30, 2024
Язык: Английский
Процитировано
0