What inspired you to pursue aging research?
Aging is the greatest risk factor for nearly all chronic diseases—from cancer to neurodegeneration—yet the biological mechanisms that convert this risk into disease remain incompletely understood. As a cell biologist, I study cellular senescence, a stress-induced program that permanently halts cell proliferation to suppress tumorigenesis. However, senescent cells develop a complex secretory phenotype, known as the senescence-associated secretory phenotype (SASP), which dramatically reshapes the tissue microenvironment. Over time, the accumulation of SASP-producing senescent cells drives sterile inflammation and tissue degeneration—key hallmarks of aging. My research aims to dissect the molecular pathways that govern SASP composition and regulation, with a focus on identifying druggable signaling nodes that can be selectively targeted without undermining the beneficial, tumor-suppressive roles of senescence. This work supports the development of next-generation senomorphic therapies designed to blunt the harmful effects of the SASP, offering a promising avenue to delay or prevent a broad range of age-related diseases.
In your view, what does AFAR mean to the field, and what does it mean, for you, to receive an AFAR grant now?
AFAR has been a driving force in aging research, supporting transformative science and fostering the next generation of leaders in the field. By championing foundational biology with translational potential, AFAR has helped shift aging from the margins to the forefront of biomedical research. Receiving an AFAR grant is both an honor and a strong endorsement of the scientific questions my lab is pursuing. This support empowers us to investigate how subcellular architecture and organelle communication contribute to cellular senescence and age-related inflammation—mechanisms with direct clinical relevance. The award provides not only critical resources but also the freedom, visibility, and momentum to pursue high-impact experiments at a pivotal stage in my career.
What is exciting about your research’s potential impact?
My research seeks to uncover a previously unrecognized layer of SASP (senescence-associated secretory phenotype) regulation that contributes to inflammaging. SASP encompasses the secretion of pro-inflammatory cytokines, chemokines, growth factors, and proteases by senescent cells, disrupting tissue homeostasis and driving age-related pathology. We are investigating membrane contact sites (MCSs) between the Golgi apparatus and lysosomes as spatial signaling hubs that amplify pro-inflammatory SASP expression. This work expands current models of SASP regulation—typically focused on transcriptional and epigenetic mechanisms—by highlighting the role of organelle architecture and subcellular organization in shaping inflammatory signaling. By elucidating how organelle interactions contribute to the pathogenic activity of senescent cells, we aim to identify new targets for selectively dampening chronic inflammation in aging while preserving the beneficial, tumor-suppressive functions of senescence. These insights could inform the design of next-generation senomorphic therapies that act with greater precision and reduced toxicity to extend healthspan.
How would you describe your research to a non-scientist?
As we age, some of our cells permanently stop dividing in response to stress or damage—a process called cellular senescence. This is the body’s natural defense against cancer, as it prevents damaged cells from growing uncontrollably. However, over time, these senescent cells begin to release harmful signals that trigger inflammation and contribute to aging and diseases like arthritis, heart disease, and dementia. My research focuses on understanding how these harmful signals are turned on. We’ve discovered that tiny contact points between two structures inside the cell—the Golgi and the lysosome—may act like communication hubs that help activate this damaging response. With support from AFAR, we’re using cutting-edge tools to map these contact sites and figure out how they control inflammation. The long-term goal is to develop ways to block the harmful effects of senescent cells while preserving their ability to prevent cancer. This could lead to safer, more targeted treatments that reduce inflammation and help people stay healthier as they age.
