Skeletal muscle aging is a major determinant of locomotor function decline and reduced quality of life in elderly populations. Therefore, a better understanding of the molecular pathways involved in muscle aging is of prime importance. Furthermore, every tissue in the body contains resident macrophages that are key regulators of tissue homeostasis. In skeletal muscle, these resident macrophages have been involved in muscle repair and regeneration upon acute injury, but their specific roles in muscle aging remain uncharted and largely overlooked. Moreover, the precise mechanisms underlying the crosstalk between muscles and macrophages also remain poorly understood. It has been observed that these cells also undergo age-related phenotypic changes, leading to chronic low-grade inflammation and impaired tissue repair, a phenomenon known as inflammaging.

In particular, it is unclear how muscle-derived signals influence macrophage behavior over time, or how macrophages modulate muscle fiber maintenance.

Ultimately through this PhD project, I aim to uncover novel mechanisms governing muscle aging and characterize the bi-directional cross-talk between skeletal muscles and innate immune macrophages during aging, using Drosophila as an integrative model which has the potential to elucidate conserved mechanisms that could lead to new therapeutic strategies to mitigate age-related muscle decline in humans.