Energy Metabolism and Brain Aging: Strategies to Delay Neuronal Degeneration

Cellular and Molecular Neurobiology, Journal Year: 2025, Volume and Issue: 45(1)

Published: April 21, 2025

Abstract Aging is characterized by a gradual decline in physiological functions, with brain aging being major risk factor for numerous neurodegenerative diseases. Given the brain’s high energy demands, maintaining an adequate ATP supply crucial its proper function. However, advancing age, mitochondria dysfunction and deteriorating metabolism lead to reduced overall production impaired mitochondrial quality control (MQC). As result, promoting healthy has become key focus contemporary research. This review examines relationship between aging, highlighting connection MQC metabolism, proposes strategies delay targeting metabolism.

Language: Английский

HSP90 N-terminal inhibition promotes mitochondria-derived vesicles related metastasis by reducing TFEB transcription via decreased HSP90AA1-HCFC1 interaction in liver cancer

Autophagy, Journal Year: 2024, Volume and Issue: unknown

Published: Oct. 26, 2024

Cancer cells compensate with increasing mitochondria-derived vesicles (MDVs) to maintain mitochondrial homeostasis, when canonical MAP1LC3B/LC3B (microtubule associated protein 1 light chain 3 beta)-mediated mitophagy is lacking. MDVs promote the transport of components into extracellular (EVs) and induce tumor metastasis. Although HSP90 (heat shock 90) chaperones hundreds client proteins its inhibitors suppress tumors, inhibitors-related chemotherapy unexpected Herein, we find that inhibitor causes damage but stimulates low LC3-induced release MDVs-derived EVs. However, why LC3 decreases what transcriptional regulatory mechanism formation under inhibition remain unknown. Because TFEB (transcription factor EB) most important transcription factor, HCFC1 (host cell C1) regulates

Language: Английский