Tohoku University · Medicine
Professor Kuniyasu Niizuma's research lab focuses on the molecular mechanisms underlying neuronal cell death following brain ischemia and stroke, with a particular emphasis on mitochondrial dysfunction, oxidative stress, and the role of key signaling proteins such as PUMA and the PIDDosome complex in delayed neuronal death. The lab investigates novel therapeutic targets and regenerative strategies, including the use of Muse cells—pluripotent stem cells with immune privilege and tissue-homing capabilities—for stroke recovery. Their work bridges basic neuroscience with translational applications, aiming to develop effective treatments for acute brain injuries and neurodegenerative conditions.
Figures are computed from collected data and may differ slightly.
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
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