九州大学 · 生化学・遺伝学・分子生物学
Nishida教授の研究室では、心筋の細胞死・萎縮・老化に深く関与するミトコンドリア動態と細骨格系のクロストーク、特にドリル1（Drp1）やTRPC3チャネルを介した酸化的なシグナル伝達機構を解明しています。心筋梗塞後の心筋細胞の老化やがん化学療法に伴う心筋萎縮のメカニズムを、細胞内シグナル伝達と細胞骨格の相互作用から解き明かしています。特に、ミトコンドリアの分裂・融合の制御と酸化的ストレスの関連性に注目し、心不全の予防的・治療的戦略の基盤を構築することを目的としています。
Figures are computed from collected data and may differ slightly.
Defective mitochondrial dynamics through aberrant interactions between mitochondria and actin cytoskeleton is increasingly recognized as a key determinant of cardiac fragility after myocardial infarction (MI). Dynamin-related protein 1 (Drp1), a mitochondrial fission-accelerating factor, is activated locally at the fission site through interactions with actin. Here, we report that the actin-binding protein filamin A acted as a guanine nucleotide exchange factor for Drp1 and mediated mitochondria
The angiotensin (Ang) type 1 receptor (AT1R) promotes functional and structural integrity of the arterial wall to contribute to vascular homeostasis, but this receptor also promotes hypertension. In our investigation of how Ang II signals are converted by the AT1R from physiological to pathological outputs, we found that the purinergic P2Y6 receptor (P2Y6R), an inflammation-inducible G protein (heterotrimeric guanine nucleotide-binding protein)-coupled receptor (GPCR), promoted Ang II-induced hy
Myocardial atrophy is a wasting of cardiac muscle due to hemodynamic unloading. Doxorubicin is a highly effective anticancer agent but also induces myocardial atrophy through a largely unknown mechanism. Here, we demonstrate that inhibiting transient receptor potential canonical 3 (TRPC3) channels abolishes doxorubicin-induced myocardial atrophy in mice. Doxorubicin increased production of ROS in rodent cardiomyocytes through hypoxic stress-mediated upregulation of NADPH oxidase 2 (Nox2), which
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