Hokkaido University · Medicine
Professor Takako Chikenji's research lab focuses on the pathophysiology of fibrotic and autoimmune rheumatic diseases, with a central emphasis on the role of growth factors such as TGF-β and CTGF in tissue fibrosis, particularly in carpal tunnel syndrome and systemic lupus erythematosus. The lab investigates the interplay between cellular senescence, immune cell infiltration, and microenvironment remodeling in chronic inflammatory and fibrotic conditions, including rheumatoid arthritis and cutaneous lupus erythematosus. A key research direction involves exploring neuro-immune interactions, especially autonomic nervous system damage in SLE, and evaluating neuroprotective therapies to mitigate systemic organ damage. The lab also examines mesenchymal stem cell-mediated tissue repair mechanisms in fibrotic and inflammatory microenvironments.
Figures are computed from collected data and may differ slightly.
Non-inflammatory fibrosis of the subsynovial connective tissue (SSCT) is a hallmark of carpal tunnel syndrome (CTS). The etiology of this finding and its relationship to the development of CTS remain poorly understood. Recent studies have found that transforming growth factor-β (TGF-β) plays a central role in fibrosis. The purpose of this study was to investigate the expression of TGF-β and connective tissue growth factor (CTGF), a downstream mediator of TGF-β, in the pathogenesis of CTS. We com
MSCs may exert their effect by remodelling the chronic inflammatory environment via senescence-related regenerative processes.
Rheumatoid arthritis (RA) is an autoimmune disease caused by inflammation of the synovium and characterized by chronic polyarthritis that destroys bone and cartilage. Fibroblast-like synoviocytes (FLSs) in the synovium of patients with RA can promote cartilage and bone destruction by producing proteins such as matrix metalloproteinases and receptor activator of NF-κB ligand, thereby representing an important therapeutic target for RA. FLSs have several phenotypes depending on which cell surface
Carpal tunnel syndrome (CTS) is an idiopathic disease that results from increased fibrosis of the subsynovial connective tissue (SSCT). A recent study found overexpression of both transforming growth factor-β (TGF-β) and connective tissue growth factor (CTGF) in the SSCT of CTS patients. This study investigated TGF-β and CTGF expression in a rabbit model of CTS, in which SSCT fibrosis is induced by a surgical injury. Levels of TGF-β1 and CTGF at 6, 12, 24 weeks after injury were determined by im
Up to 60% of patients with systemic lupus erythematosus (SLE) experience autonomic symptom. Sympathetic nervous system damage can cause dysfunction of the bone marrow that activates inflammatory cells, potentially causing multiple organ damage. We hypothesized that sympathetic nervous system damage would induce bone marrow dysfunction with multiple organ damage in SLE, and that multiple organ damage could be improved by therapy targeting the nervous system. Here, we showed that damage to autonom
Senescent cells create a microenvironment that directs cytotoxic T cell-mediated responses against normal epidermis in patients with CLE, contributing to disease pathology. Targeting senescent cells and their signaling pathways may offer novel therapeutic strategies for patients with skin lesions from CLE and SLE.
The purpose of this study was to investigate the strengths of four intrinsic muscles of the hand of college baseball players. The strengths of four intrinsic muscle groups were measured by the Rotterdam Intrinsic Hand Myometer (RIHM) which has been developed to assess the abduction of the little finger and index finger, and palmar abduction and opposition of the thumb. The strengths of these four intrinsic muscle groups were compared between baseball players and inexperienced sports players. The
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