Overview
Cellular senescence — a hallmark of aging — is a state of irreversible proliferative arrest driven by cellular stress. Senescent cells exhibit a senescence-associated secretory phenotype (SASP) comprising pro-inflammatory cytokines, chemokines, proteases, and other factors that promote chronic inflammation and tissue dysfunction. Because senescent cells accumulate with age and are long-lived, they are repeatedly exposed to physiological stressors, each of which could reshape their secretory output and amplify their detrimental paracrine effects on surrounding tissues.
A central question in the field is how the stress response is wired in senescent cells relative to healthy ones, and whether these differences can be therapeutically exploited. The lab studies the basic molecular mechanisms of stress response — from RNA stability and decay to translational regulation — and how these programs are rewired in senescence and aging. To do so, the lab combines proteomics, label-based mass spectrometry, ribosome profiling, long-read nanopore sequencing, and machine learning to capture the coordinated interaction of translational and transcriptional programs at single-molecule resolution.