慶應義塾大学 · 医学
Yoshinori Katsumata教授の研究室は、心筋細胞におけるプロスタグランジンD2の代謝経路とグルココルチコイドの心筋保護作用に注目し、虚血再灌流障害に対する心機能の維持機構を解明しています。特に、L-プロスタグランジンD合成酵素（L-PGDS）を介したPGD2産生が心筋細胞に与えるシグナル伝達経路の制御機構を、遺伝子発現ネットワークの観点から解析しています。また、臨床的応用の可能性も視野に入れ、PCIにおける心筋保護戦略の開発にも貢献しています。
Figures are computed from collected data and may differ slightly.
We recently demonstrated that glucocorticoids markedly upregulate the expression of cyclooxygenase-2 in cardiomyocytes and protect hearts from ischemia-reperfusion (I/R) injury by activating lipocalin-type prostaglandin D (PGD) synthase (L-PGDS)-derived PGD(2) biosynthesis. We examined a downstream mechanism of cardioprotection elicited by PGD(2) biosynthesis. Acute PGD(2) treatment did not protect hearts against I/R injury. We then speculated that PGD(2) and its metabolite 15-deoxy-Δ12,14-PGJ(2
The first clinical study has shown that HI during PCI is feasible and safe and may also promote LV reverse remodeling at 6 months after STEMI. The study was not powered to test efficacy and a further large-scale trial is warranted. (Clinical trials registration: UMIN00006825).
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