James Wordsworth

Why we age: the four process model

The paper proposes a four-process model of ageing that connects DNA damage, metabolic slowdown, and cellular selection to explain age-related diseases and the evolutionary basis of ageing.

Metabolic slowdown as the proximal cause of ageing and death

This paper connects metabolic slowdown to ageing and age-related diseases through a fuel and energy model, explaining anti-ageing interventions and paradoxes of ageing.

Transcriptomic and epigenetic assessment of ageing female skin and fibroblasts identifies age related reduced oxidative phosphorylation is exacerbated by smoking.

Transcriptomic and epigenetic assessment of ageing male skin identifies disruption of Ca2+ homeostasis; exacerbated by smoking and UV exposure

This study identifies age-related disruptions in calcium homeostasis in male skin fibroblasts, exacerbated by smoking and UV exposure, and links these changes to increased senescence and disease susceptibility.

Systematic transcriptomic analysis and temporal modelling of the senescent human fibroblast

The paper systematically analyzes transcriptomic data from human fibroblasts to identify gene expression patterns associated with different senescence types and models temporal protein changes.

Cell Senescence-Independent Ageing of Human Skin

The paper shows that while senescent cells contribute to collagen degradation with age, reduced collagen production in adult skin is due to senescence-independent processes.