Related Experiment Video
Updated: May 4, 2026

An Adoptive Transfer Model of Rheumatoid Arthritis in Mice
Published on: June 6, 2025
What can we learn from Werner syndrome? A biased view from a rheumatologist
1Department of Rheumatology, Tokyo Metropolitan Ohtsuka Hospital , 2-8-1 Minami-Otsuka, Toshima-ku, Tokyo 170-0005 , Japan.
Abstract:
Abstract Werner syndrome (WS), caused by the mutation of the RecQ3 DNA helicase gene (loss of function), manifests scleroderma-like skin changes and juvenile cataracts in addition to a variety of clinical and biochemical aging phenotypes at an early stage of life, followed by death at an average age of 46 years. WS has been nominated as a top-ranking premature aging syndrome, or a human model of accelerated aging. Analyses of clinical and biological deterioration of body systems observed in WS may shed a unique light on the role of gene(s) in the pathogenesis of systemic sclerosis (SSc) and normal human aging.
Related Concept Videos
Rheumatic Heart Disease I: Introduction
Rheumatic Heart Disease III: Medical Management
Genome-wide Association Studies-GWAS
GWAS does not require the identification of the target gene involved in...
Rheumatic Heart Disease II: Clinical Manifestations and Diagnostic Studies
Rheumatic Heart Disease IV: Nursing Management
Bias in Epidemiological Studies

