Gallic acid and loganic acid attenuate amyloid-β oligomer-induced microglia damage via NF-КB signaling pathway DOI
Yandong Ma, Huan Liu,

Qian Chen

et al.

Neuropharmacology, Journal Year: 2024, Volume and Issue: 263, P. 110215 - 110215

Published: Nov. 12, 2024

Language: Английский

Oxidative Stress and Mitochondrial Impairment: Key Drivers in Neurodegenerative Disorders DOI

Pei Wen,

Zhixin Sun,

Fengting Gou

et al.

Ageing Research Reviews, Journal Year: 2025, Volume and Issue: unknown, P. 102667 - 102667

Published: Jan. 1, 2025

Language: Английский

Citations

1

Mitochondria at the crossroads: Quality control mechanisms in neuronal senescence and neurodegeneration DOI Creative Commons

Yifei Zheng,

Jiahui Yang,

Xuanyao Li

et al.

Neurobiology of Disease, Journal Year: 2025, Volume and Issue: unknown, P. 106862 - 106862

Published: March 1, 2025

Mitochondria play a central role in essential cellular processes, including energy metabolism, biosynthesis of metabolic substances, calcium ion storage, and regulation cell death. Maintaining mitochondrial quality control is critical for preserving health ensuring function. Given their high demands, neurons depend on effective to sustain functionality. Neuronal senescence, characterized by progressive decline structural integrity function, hallmark neurodegenerative diseases. In senescent neurons, abnormal morphology, functional impairments, increased reactive oxygen species production disrupted mechanisms are frequently observed. Understanding the pathological changes neuronal structure, exploring intricate relationship between health, leveraging interventions provide promising foundation addressing age-related This review highlights key control, biogenesis, dynamics, ubiquitin-proteasome system, autophagy pathways, mitochondria-derived vesicles, inter-organelle communication, while discussing roles senescence potential therapeutic strategies. These insights may pave way innovative treatments mitigate disorders.

Language: Английский

Citations

0

A New Perspective on the Role of Alterations in Mitochondrial Proteins Involved in ATP Synthesis and Mobilization in Cardiomyopathies DOI Open Access
Melissa Vázquez-Carrada, María Magdalena Vilchis‐Landeros, Héctor Vázquez‐Meza

et al.

International Journal of Molecular Sciences, Journal Year: 2025, Volume and Issue: 26(6), P. 2768 - 2768

Published: March 19, 2025

The heart requires a continuous energy supply to sustain its unceasing contraction–relaxation cycle. Mitochondria, double-membrane organelle, generate approximately 90% of cellular as adenosine triphosphate (ATP) through oxidative phosphorylation, utilizing the electrochemical gradient established by respiratory chain. Mitochondrial function is compromised damage mitochondrial DNA, including point mutations, deletions, duplications, or inversions. Additionally, disruptions proteins associated with membranes regulating metabolic homeostasis can impair chain’s efficiency. This results in diminished ATP production and increased generation reactive oxygen species. review provides an overview mutations affecting transporters involved synthesis, particularly those synthesis mobilization, it examines their role pathogenesis specific cardiomyopathies.

Language: Английский

Citations

0

The associations between brain aging and mitochondria dysfunction: Mechanism and intervention strategies DOI
Yi Rong

Deleted Journal, Journal Year: 2025, Volume and Issue: unknown, P. 1 - 16

Published: April 20, 2025

Brain aging, an exquisitely intricate biological phenomenon, is intertwined with cognitive deterioration and the pathogenesis of neurodegenerative maladies. Mitochondria, cellular powerhouses responsible for energy homeostasis, assume a central indispensable role in this process. This review delves deeply into multifaceted associations between mitochondrial dysfunction brain encompassing perturbations metabolism, exacerbation oxidative stress, aberrations dynamics, activation inflammatory response, DNA mutations, all which interact complex network to drive progression aging. Simultaneously, it undertakes meticulous dissection functions some key mitochondria-related molecules In terms intervention strategies, emerging evidence suggests that inhibition cyclic GMP-AMP synthase-stimulator interferon genes (cGAS-STING) signaling axis holds promise alleviating phenotypes senescent cells tissues. Downregulating levels relevant transfer RNA-derived small RNAs (tsRNAs) represents potential approach safeguard crucial processes. Supplementation spermidine spermine has demonstrated efficacy ameliorating function performance. Moreover, comprehensive paradigms targeting antioxidative stress responses, autophagy regulation offer avenues retarding Collectively, existing body research furnishes profound insights underlying mechanisms aging serves as bedrock development efficacious modalities. Future imperatives should center on elucidating molecular mechanisms, formulating highly precise expediting translation basic findings clinical applications. utmost significance enhancing quality life elderly forestalling onset diseases.

Language: Английский

Citations

0

Gallic acid and loganic acid attenuate amyloid-β oligomer-induced microglia damage via NF-КB signaling pathway DOI
Yandong Ma, Huan Liu,

Qian Chen

et al.

Neuropharmacology, Journal Year: 2024, Volume and Issue: 263, P. 110215 - 110215

Published: Nov. 12, 2024

Language: Английский

Citations

0