Daryl P. Shanley

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.

The paper introduces tools for parameter estimation of biochemical networks using stability constraints, validated on MTOR network data from breast cancer cells.

The paper develops a multi-scale computational model of wound healing that simulates senescent cell dynamics and SASP profiles to understand their role in tissue repair and disease states.

The paper identifies miR-199a/b-5p as pro-chondrogenic regulators and constructs a multi-miRNA kinetic model of chondrogenesis.

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.

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.

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.

The paper argues that biological ageing involves a decrease in cellular sensitivity and information transmission due to accumulated damage, leading to increased noise in biological networks.