Tohoku University · 의학
니이즈마 쿠니야수 교수의 연구실은 뇌질환, 특히 뇌경색과 심정지 이후 신경세포 사멸 메커니즘을 중심으로 산화 스트레스, 미토콘드리아 기능 이상, 그리고 세포 사멸 신호 경로(예: PIDD오소드, PUMA, p53)의 역할을 규명하고 있습니다. 특히 퇴행성 뇌질환과 뇌허혈 후 손상에서의 분자적 기전을 밝히고, 이를 바탕으로 신경보호 및 재생 치료 전략을 개발하고 있습니다. 최근에는 Muse 세포를 이용한 줄기세포 치료도 진행하며, 이식 후 손상 부위에 선택적 향유 및 기능 회복을 목표로 하고 있습니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
Mitochondria are the powerhouse of the cell. Their primary physiological function is to generate adenosine triphosphate through oxidative phosphorylation via the electron transport chain. Reactive oxygen species generated from mitochondria have been implicated in acute brain injuries such as stroke and neurodegeneration. Recent studies have shown that mitochondrially-formed oxidants are mediators of molecular signaling, which is implicated in the mitochondria-dependent apoptotic pathway that inv
The area with prolonged RRT colocalized with atherosclerotic change on the aneurysm wall. Male sex and maximum RRT were independent risk factors for atherogenesis in intracranial aneurysms.
These results imply a potential role for PUMA in delayed CA1 neuronal death after tGCI and that it could be a molecular target for therapy.
A brief period of global brain ischemia, such as that induced by cardiac arrest or cardiopulmonary bypass surgery, causes cell death in vulnerable hippocampal CA1 pyramidal neurons days after reperfusion. Although numerous factors have been suggested to account for this phenomenon, the mechanisms underlying it are poorly understood. We describe a cell death signal called the PIDDosome, a protein complex of p53-induced protein with a death domain (PIDD), receptor-interacting protein-associated IC
Effective treatments for stroke after the acute phase remain elusive. Muse cells are endogenous, pluripotent, immune-privileged stem cells capable of selectively homing to damaged tissue after intravenous injection and replacing damaged/lost cells via differentiation. This randomized, double-blind, placebo-controlled trial enrolled ischemic stroke patients with modified Rankin Scale (mRS) ≥3. Randomized patients received a single intravenous injection of an allogenic Muse cell-based product, CL2
