Ryo Higuchi‐Sanabria

Constitutive somatic expression of four tardigrade disordered proteins shortened C. elegans lifespan and healthspan and gave little stress protection. Three of the four reduced polyQ aggregation under hyperosmotic stress.

This study investigates how actin structure and function affect aging in C. elegans and finds that actin dysfunction accelerates aging hallmarks and correlates with human age-related decline in gait speed.

This study shows heat stress activates UPRER through XBP-1 and HSF-1 in C. elegans, with cross-talk to cytosolic HSR and inter-tissue stress communication enhancing thermotolerance.

The paper identifies senescent fibroblast heterogeneity in IPF and links it to DNA damage response dysregulation using gene expression analysis.

The paper develops a fluorescent biosensor to measure methionine dynamics with high spatiotemporal resolution and applies it to study methionine metabolism in cells and in vivo.

This study shows DNA damage in neurons leads to a senescent-like state similar to Alzheimer's disease, with distinct features from fibroblasts.

This study maps age- and sex-related lipid changes across 10 mouse organs, revealing organ-specific and sex-dependent patterns in the lipidome during aging.

This study maps metabolic changes in 12 organs of male and female mice across 5 ages, identifying sex-specific patterns and a metabolic aging clock.

The paper identifies distinct roles of GABAergic, glutamatergic, and octopaminergic neurons in mediating non-autonomous UPRER through transcriptomic and functional analyses in C. elegans.

This study uses RNA-sequencing to analyze transcriptomic changes in C. elegans under different mitochondrial stressors that activate UPRmt, aiming to determine if specific transcriptomic changes correlate with longevity.

This study compares mitochondrial imaging strategies in C. elegans during aging, evaluating transgenic constructs for mitochondrial morphology analysis.

The paper examines iron levels and lipid peroxidation in DSAD brains, finding increased iron and lipid damage compared to AD and controls, suggesting ferroptosis involvement.

The paper investigates iron-mediated toxicity in Alzheimer's disease by analyzing postmortem brain tissue and ApoE4 mice, finding increased lipid peroxidation and decreased antioxidants in lipid rafts, which are reduced by iron chelation.

This study investigates the impact of substrate stiffness on C. elegans health and longevity, finding only mild effects on cellular and organismal health.

This study shows glial cells in C. elegans sense mitochondrial stress and signal to neurons to improve protein homeostasis and longevity.

This study identifies SKN-1 as a metabolic surveillance factor that responds to amino acid catabolism to influence stress resistance in C. elegans.