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Central damage and sensory deprivation caused by noise-induced hearing loss in the pre-symptomatic Alzheimer's disease (AD) phase can compromise auditory cortex-hippocampal circuitry, targeting common pathogenetic pathways, thereby accelerating onset and progression of AD phenotype.

As worms age reduced glutathione together with increased ferrous iron increases frailty and leads to ferroptosis, which is amenable to therapeutic intervention.

The neutral amino acid transporter SLC38A2 is an essential protective factor for renal medulla during urine concentration.

Genome-scale integration of transposon mutagenesis with a redox biosensor identified a hypothetical transcription factor- Rv0158 required to calibrate the growth, cytoplasmic redox potential, and respiration of Mycobacterium tuberculosis in response to metabolic switching from glucose to fatty acids.

Moderate exercise upregulated compensatory antioxidant capability and reached a high-level redox balance, whereas antioxidant intervention achieved a low-level redox balance by inhibiting oxidative stress for treating diabetes.

Enteroendocrine cells sense nutrients in the gut and regulate digestive physiology but are rendered insensitive following fat ingestion due to alteration of gut microbiota.

¹H-Magnetic resonance spectroscopy at 14T reveals a metabolic signature for anti-depressant-like effects of acetyl-L-carnitine in nucleus accumbens of susceptible mouse.

Genome-wide CRISPRi screens and proteome profiling of lysosomes link lipid dysregulation to ESCRT disruption and proteostasis defect.

Ferroptotic stress enhances the accumulation of damage-associated inflammatory proximal tubular cell state, thereby promoting maladaptive renal repair and the AKI-to-CKD transition.

A comprehensive molecular description of the cellular transition into replicative senescence provides evidence of metabolic, epigenetic, and regulatory rewiring that links senescence with wound healing and fibrosis.