With the advent of translational research, the field of biomedical science has been evolving beyond the mechanistic understanding of biological phenomena and disease pathogenesis, advancing toward an innovative and integrative form of future medicine aimed at treating previously intractable diseases. Alongside this scientific progress, the hypothesis that inflammation serves as a common origin for autoimmune diseases, metabolic disorders, and cancer has gained widespread support.

Our laboratory was among the first to identify that mitochondrial damage, triggered by various forms of stress, can act as a primary driver of inflammatory responses. Building on this foundational discovery, we are leading diverse research efforts to develop novel therapeutic strategies targeting inflammation in the context of autoimmune disorders, metabolic diseases, and cancer.

Inflammation Ignited: The Hidden Role of Mitochondrial DNA

Chronic inflammation-induced injury drives tissue fibrosis, compromising organ parenchyma and potentially leading to organ failure. Liver fibrosis resulting from chronic hepatitis is a well-known example of this process. Our lab discovered that mtDNA released into the cytosol under stress acts as an upstream trigger of fibrosis. We identified a novel protein that is activated by mtDNA and promotes the expression of inflammatory and fibrogenic genes, particularly in hepatic stellate cells—the main effectors of liver fibrosis.In a mouse model, inhibiting this protein reduced both inflammation and extracellular matrix accumulation. These findings reveal a previously unrecognized mitochondrial pathway driving fibrosis and suggest new therapeutic strategies targeting mtDNA-induced signaling.