Lattice Percolation Approach to 3D Modeling of Tissue Aging

TL;DR

This paper introduces a 3D lattice percolation model to simulate tissue aging, revealing how senescent cells influence tissue stability and lifespan, supported by statistical mechanics and experimental validation.

Contribution

It presents a novel 3D percolation-based modeling approach for tissue aging, highlighting the role of senescent cells in tissue connectivity and lifespan extension.

Findings

Senescent cells can form a second infinite cluster in 3D tissues.

Inhibition of senescence may extend tissue lifespan.

3D models show different connectivity effects compared to 2D.

Abstract

We describe a 3D percolation-type approach to modeling of the processes of aging and certain other properties of tissues analyzed as systems consisting of interacting cells. Lattice sites are designated as regular (healthy) cells, senescent cells, or vacancies left by dead (apoptotic) cells. The system is then studied dynamically with the ongoing processes including regular cell dividing to fill vacant sites, healthy cells becoming senescent or dying, and senescent cells dying. Statistical-mechanics description can provide patterns of time dependence and snapshots of morphological system properties. The developed theoretical modeling approach is found not only to corroborate recent experimental findings that inhibition of senescence can lead to extended lifespan, but also to confirm that, unlike 2D, in 3D senescent cells can contribute to tissue's connectivity/mechanical stability. The latter effect occurs by senescent cells forming the second infinite cluster in the regime when the regular (healthy) cell's infinite cluster still exits.