Our group has so far reported the pathogenic role of cellular senescence and systemic insulin resistance in age-related cardiovascular-metabolic disorders including heart failure, atherosclerotic diseases, obesity and diabetes. “Metabolic remodeling” is one of the keywords for aging research, and studies with brown adipose tissue showed maintaining the homeostasis of this organ as crucial to combat obesity or heart failure. Through these studies, I came to consider the mechanisms contributing for the synchronization of aging (sync-aging) as interesting. Now, we define “senometabolite” or “senoprotein” as circulating molecules having causal roles for the sync-aging. Based on several unpublished data, I am now trying to establish new concepts for diseases; One is Age-related fibrotic disorders (A-FiD), and another is Senometabolite Related Disorders (SRDs). Together with the suppression of sync-aging, we are also trying to establish a method to reverse aging with the senolytic approach.