The role of TRAP1 in regulating mitochondrial dynamics during acute hypoxia-induced brain injury DOI Creative Commons

Fengying Liu,

Xueyang Lin,

Xiaodong Wu

et al.

Journal of Translational Medicine, Journal Year: 2024, Volume and Issue: 22(1)

Published: Oct. 28, 2024

Brain damage caused by acute hypoxia is associated with the physiological activities of mitochondria. Although mitochondria being dynamically regulated, our comprehensive understanding response specific brain cell types to remains ambiguous. Tumor necrosis factor receptor-associated protein 1 (TRAP1), a mitochondrial-based molecular chaperone, plays role in controlling mitochondrial movements. Herein, we demonstrated that significantly alters morphology and functionality both vivo vitro injury experiments. Summary-data-based Mendelian Randomization (SMR) analyses revealed possible causative links between mitochondria-related genes injury. Advancing protein-protein interaction network docking further elucidated associations TRAP1 dynamics. Furthermore, it was shown knockdown levels variably affected expression key dynamics proteins (DRP1, FIS1, MFN1/2) primary hippocampal neurons, astrocytes, BV-2 cell, leading changes structure function. Understanding function altering activity during hypoxia-induced could help serve as potential therapeutic target mitigate neurological damage.

Language: Английский

Targeting Mitochondrial Dysfunction in Cerebral Ischemia: Advances in Pharmacological Interventions DOI Creative Commons
И. Ф. Беленичев, Olena Popazova, Nina Bukhtiyarova

et al.

Antioxidants, Journal Year: 2025, Volume and Issue: 14(1), P. 108 - 108

Published: Jan. 18, 2025

The study of mitochondrial dysfunction has become increasingly pivotal in elucidating the pathophysiology various cerebral pathologies, particularly neurodegenerative disorders. Mitochondria are essential for cellular energy metabolism, regulation reactive oxygen species (ROS), calcium homeostasis, and execution apoptotic processes. Disruptions function, driven by factors such as oxidative stress, excitotoxicity, altered ion balance, lead to neuronal death contribute cognitive impairments several brain diseases. Mitochondrial can arise from genetic mutations, ischemic events, hypoxia, other environmental factors. This article highlights critical role progression diseases discusses need targeted therapeutic strategies attenuate damage, restore enhance neuroprotection.

Language: Английский

Citations

2
Phosphoglycerate kinase 1 as a therapeutic target in neurological disease DOI Creative Commons
Harriet McHale-Owen, Kiterie M. E. Faller, Helena Chaytow

et al.

Trends in Molecular Medicine, Journal Year: 2025, Volume and Issue: unknown

Published: April 1, 2025

Language: Английский

Citations

0
The role of TRAP1 in regulating mitochondrial dynamics during acute hypoxia-induced brain injury DOI Creative Commons

Fengying Liu,

Xueyang Lin,

Xiaodong Wu

et al.

Journal of Translational Medicine, Journal Year: 2024, Volume and Issue: 22(1)

Published: Oct. 28, 2024

Brain damage caused by acute hypoxia is associated with the physiological activities of mitochondria. Although mitochondria being dynamically regulated, our comprehensive understanding response specific brain cell types to remains ambiguous. Tumor necrosis factor receptor-associated protein 1 (TRAP1), a mitochondrial-based molecular chaperone, plays role in controlling mitochondrial movements. Herein, we demonstrated that significantly alters morphology and functionality both vivo vitro injury experiments. Summary-data-based Mendelian Randomization (SMR) analyses revealed possible causative links between mitochondria-related genes injury. Advancing protein-protein interaction network docking further elucidated associations TRAP1 dynamics. Furthermore, it was shown knockdown levels variably affected expression key dynamics proteins (DRP1, FIS1, MFN1/2) primary hippocampal neurons, astrocytes, BV-2 cell, leading changes structure function. Understanding function altering activity during hypoxia-induced could help serve as potential therapeutic target mitigate neurological damage.

Language: Английский

Citations

2