Kyushu University · 생화학·유전·분자생물학
Motohiro Nishida 교수의 연구실은 심장 및 혈관 질환에서 세포 구조와 기능의 변화를 중심으로 한 기전 연구를 수행하고 있습니다. 특히 미토콘드리아 운동 조절, 세분화 및 산화 스트레스와 관련된 단백질 상호작용이 심부전, 심근경화 후 심장 취약성, 고혈압 등에서 어떻게 기여하는지 규명하고 있습니다. TRPC3-Nox2 복합체나 Filamin A-Drp1 상호작용 등 세포 내 신호전달 경로의 정밀한 메커니즘을 밝혀내는 데 초점을 맞추고 있습니다. 이는 심장질환의 새로운 치료 타겟을 제시하는 데 기여하고 있습니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
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
