Chronic inflammation has emerged as a common pathological feature shared by obesity, lifestyle-related diseases, and cancer. It can be regarded as a condition in which inflammation, initially triggered as a protective response to various stresses, fails to resolve properly and instead persists over time. However, the mechanisms by which inflammation becomes chronic remain incompletely understood.

To address this question, we focus on macrophages, which play a central role in the development of chronic inflammation. By integrating molecular biological approaches with cutting-edge transcriptomic and epigenomic analyses, we aim to elucidate the mechanisms that drive the persistence of inflammatory responses. In particular, we are interested in the tight coupling between immune responses and cellular metabolism in macrophages, and we seek to develop novel therapeutic and preventive strategies targeting macrophage metabolism in chronic inflammatory conditions.

More recently, chronic inflammation has been implicated not only in lifestyle-related diseases but also in a broader range of conditions, including chronic endometritis associated with infertility, noise-induced hearing loss, and impaired wound healing. In collaboration with clinicians across multiple specialties, we are working to elucidate the underlying mechanisms of these conditions and to develop innovative therapeutic approaches.

Skeletal muscle plays essential roles not only in locomotion and posture maintenance but also as the largest metabolic organ responsible for systemic glucose homeostasis. Muscle atrophy caused by physical inactivity, prolonged immobilization, or aging leads not only to a decline in physical function but also to an increased risk of lifestyle-related diseases, ultimately exerting a profound impact on quality of life. Age-associated loss of muscle mass and strength, termed sarcopenia, has become an increasingly serious health issue in aging societies such as Japan.

In contrast, skeletal muscle possesses a remarkable capacity for regeneration. Following muscle injury, muscle stem cells—known as satellite cells—play a central role in the regenerative process. These cells normally reside in a quiescent state but become activated upon injury, proliferate and differentiate, and ultimately give rise to new muscle fibers. In addition, satellite cells self-renew to maintain their population, thereby preserving tissue homeostasis and regenerative potential.

Muscle injury is also accompanied by a robust inflammatory response, during which various immune cells accumulate in the damaged tissue. Notably, depletion of macrophages severely impairs muscle regeneration, highlighting their critical role in the repair process.

Based on this background, we focus on the interactions between immune cells—including macrophages—and satellite cells. Using cutting-edge approaches such as single-cell analysis, we aim to elucidate the coordinated regulatory mechanisms that integrate inflammation and regeneration following muscle injury. Ultimately, our goal is to establish a foundation for the development of preventive and therapeutic strategies for sarcopenia.