Aging presents various complications, among which fibrotic diseases emerge as one of the most prevalent, claiming a staggering 30% of lives in the western world. Fibrosis can affect diverse organs, leading to a gradual replacement of functional tissues by scar tissue composed of extracellular matrix, myofibroblasts, and senescent cells, severely compromising organ function and ultimately leading to death.
Despite their pervasive impact, the clinical care for patients with fibrotic diseases remains unresolved due to a lack of understanding of their pathobiology, the absence of effective treatment modalities, and the scarcity of early detection technologies.
Our recent investigations have highlighted an unexpected causative link between disrupted iron metabolism and the pathobiology of fibrosis. We have found an important role for aberrant iron accumulation, not only fueling fibrogenesis but also contributing to the maturation of senescent cells. These findings have significant implications for the development of novel diagnostic capabilities and innovative therapeutic strategies for senescence-related diseases.