Rlip76 in Ageing and Alzheimer’s Disease: Focus on Oxidative Stress and Mitochondrial Mechanisms DOI

Madhuri Bandaru,

Omme Fatema Sultana, Md. Ariful Islam

и другие.

Ageing Research Reviews, Год журнала: 2024, Номер 103, С. 102600 - 102600

Опубликована: Ноя. 30, 2024

Язык: Английский

Identification and preliminary validation of biomarkers associated with mitochondrial and programmed cell death in pre-eclampsia DOI Creative Commons
Rong Lin, Xisheng Weng, Liang Lin

и другие.

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

0

MARCH5 ameliorates aortic valve calcification via RACGAP1-DRP1 pathway associated mitochondrial quality control DOI
Jialiang Zhang, Y. Zhang, Wenhua Lei

и другие.

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research, Год журнала: 2025, Номер unknown, С. 119911 - 119911

Опубликована: Янв. 1, 2025

Язык: Английский

Процитировано

0

Harnessing exercise to combat chronic diseases: the role of Drp1-Mediated mitochondrial fission DOI Creative Commons
Yingxin Sun,

Junchen He,

Lei Bao

и другие.

Frontiers 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

0

Pre-clinical evidence for mitochondria as a therapeutic target for luteolin: a mechanistic view DOI
Marcos Roberto de Oliveira

Chemico-Biological Interactions, Год журнала: 2025, Номер unknown, С. 111492 - 111492

Опубликована: Март 1, 2025

Язык: Английский

Процитировано

0

Rlip76 in Ageing and Alzheimer’s Disease: Focus on Oxidative Stress and Mitochondrial Mechanisms DOI

Madhuri Bandaru,

Omme Fatema Sultana, Md. Ariful Islam

и другие.

Ageing Research Reviews, Год журнала: 2024, Номер 103, С. 102600 - 102600

Опубликована: Ноя. 30, 2024

Язык: Английский

Процитировано

0