Speaker
Description
Cellular aging associated with telomere shortening plays a crucial role in female fertility. Beyond the natural decline caused by the loss of telomeric repeats during cell division, additional factors such as oxidative stress (OS) can accelerate telomere erosion by inducing substantial telomeric damage. Despite its biological relevance, mathematical modeling of accelerated aging mechanisms leading to infertility remains limited in the literature.
An initial-boundary value problem based on a diffusion-advection equation has previously been proposed in \citep{portillo2023influence} to describe the evolution of a cell population experiencing a gradual reduction in proliferative potential due to the end-replication problem. Subsequently, we introduced a continuum model that accounts for random telomere shortening induced by OS in \citep{portillo2025influence} by replacing the advection term with a Caputo fractional derivative of order $\beta$, $0< \beta <1$, with respect to the generational age. The deviation of the fractional order from unity is interpreted as an oxidation parameter.
The model is applied to human follicular development from the preantral to the pre-ovulatory stage in both young and older women, allowing us to investigate the combined effects of oxidative stress and reduced telomerase activity. Our results show that increasing oxidative stress leads to an increase in the generational age of granulosa cells, indicating accelerated telomere aging.
