The University of Osaka · Medicine
Professor Kei Kamide's research lab focuses on the molecular mechanisms underlying cardiovascular and metabolic diseases, with a particular emphasis on the roles of non-coding RNAs such as ANRIL and signaling molecules like RGS2 in disease pathogenesis. The lab investigates how genetic variations and epigenetic regulation contribute to conditions including hypertension, left ventricular hypertrophy, and metabolic syndrome, often using animal models to dissect the contributions of the renin-angiotensin system and sympathetic nervous system. Current research explores the interplay between insulin resistance, local tissue RAS activation, and cardiac remodeling. The lab aims to identify novel therapeutic targets for preventing and treating cardiovascular and metabolic disorders.
Figures are computed from collected data and may differ slightly.
ANRIL is a recently discovered long non-coding RNA encoded in the chromosome 9p21 region. This locus is a hotspot for disease-associated polymorphisms, and it has been consistently associated with cardiovascular disease, and more recently with several cancers, diabetes, glaucoma, endometriosis among other conditions. ANRIL has been shown to regulate its neighbor tumor suppressors CDKN2A/B by epigenetic mechanisms and thereby regulate cell proliferation and senescence. However, the clear role of
Our results suggest that genetic variations in RGS2 contribute partly to the hypertensive phenotype.
Left ventricular hypertrophy in FFR may be less dependent on systemic elevations of BP and more dependent on the RAS and the sympathetic nervous system. Use of an AT1 receptor antagonist might be the most beneficial way to prevent progression of LVH through direct effects on tissue RAS and the sympathetic nervous system in FFR. As these changes occur in a rat model with hyperinsulinemia, insulin may have a role in promoting LVH by activating the local RAS and sympathetic nervous system activity.
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