What inspired you to pursue aging research?
My ultimate career goal is to become an independent investigator in skeletal biology with a focus on developing treatments for bone diseases such as osteoporosis, which is prevalent among the elderly, globally affecting 1 in 2 women and 1 in 4 men over 50 years of age. This pursuit is deeply personal, rooted in the profound loss of my mother and grandmother to bone diseases, yet it left me with a great sense of purpose. Since then, my motivation has been to contribute to the development of therapies with two critical purposes: (1) to prevent the development of skeletal fragilities and (2) to provide an effective treatment for bone diseases. Throughout my journey, I have studied the role of immune cells called macrophages in bone development and fracture healing. The natural progression of my research is to elucidate how macrophages specifically contribute to aging-related skeletal health decline, which will be a focus of my aging research.
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 pivotal in advancing the field of aging research. By funding groundbreaking studies, AFAR has contributed to key discoveries that have shaped our understanding of the biological mechanisms of aging and promoted the development of therapies to improve healthspan. AFAR’s support for early-career researchers has also been instrumental in cultivating new generations of scientists dedicated to the study of aging.
Receiving an AFAR grant at this stage of my career would be both an honor and a significant milestone. It would provide me with critical resources to pursue innovative research on skeletal aging, specifically investigating how immune cells like macrophages contribute to age-related bone health decline. Beyond the financial support, this grant would validate my research direction and open opportunities for collaboration with leading experts in the aging field. Ultimately, it would bring me closer to achieving my goal of developing effective therapies for aging-related bone diseases.
What is exciting about your research’s potential impact?
This project will directly address three key hallmarks of aging: cellular senescence, iron dyshomeostasis, and inflammaging. Our preliminary research highlights iron accumulation in macrophages as a critical link between these age-related processes, making it a promising target for new therapeutic interventions. We aim to leverage senolytics and iron chelators, both of which are being studied for their anti-aging potential. While these agents show promise in mitigating aging and extending healthspan, their effects on specific cell types remain largely unexplored. Our study identifies aged bone marrow macrophages as a novel target for both senolytic and iron chelation therapy. Our initial findings show that senolytics can reduce iron-laden macrophages, but eliminating these cells alone does not resolve the ongoing issue of iron retention in the body. Therefore, we propose a unique combined approach using senolytics and iron chelators. This strategy offers dual benefits: removing senescent, iron-laden macrophages and simultaneously facilitating the elimination of excess iron, preventing newly formed macrophages from suffering the same fate. This synergistic approach holds great potential for improving healthspan by addressing multiple facets of aging-related dysfunction at once.
How would you describe your research to a non-scientist?
Iron is vital for many bodily functions, including oxygen transport, energy production, and DNA synthesis. However, as we age, excessive iron can accumulate and contribute to problems such as memory decline and shorter lifespans. This is because too much iron can cause cells to die or lose their function, leading to age-related health issues. Our recent research on older mice has found that iron builds up in the bone marrow, particularly in cells called macrophages. These macrophages are essential for producing immune and red blood cells, managing inflammation, and clearing out damaged or old cells. As macrophages age, their function declines, and we suspect that iron buildup is a major factor. To address this, we are exploring a new approach that combines two therapies: one to remove excess iron and another to eliminate aged/damaged cells. This combined treatment could help clear out harmful aged cells and prevent further damage from excess iron. This research could lead to new strategies for managing for age-related conditions, using safe and well-known therapies already approved for other uses.
