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Satoshi Matsuzaki

Researcher at Oklahoma Medical Research Foundation

Publications -  32
Citations -  1536

Satoshi Matsuzaki is an academic researcher from Oklahoma Medical Research Foundation. The author has contributed to research in topics: Mitochondrion & Insulin. The author has an hindex of 17, co-authored 28 publications receiving 1274 citations. Previous affiliations of Satoshi Matsuzaki include University of Oklahoma.

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MicroRNA-214 protects the mouse heart from ischemic injury by controlling Ca²⁺ overload and cell death.

TL;DR: A pivotal role is revealed for miR-214 as a regulator of cardiomyocyte Ca²⁺ homeostasis and survival during cardiac injury, as well as repression of several downstream effectors of Ca�⁺ signaling that mediate cell death.
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Maintenance of cardiac energy metabolism by histone deacetylase 3 in mice

TL;DR: A unique role for Hdac3 in maintenance of cardiac function and regulation of myocardial energy metabolism is revealed and can be attributed to excessive activity of the nuclear receptor PPARalpha.
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Insulin-like growth factor receptor signaling regulates working memory, mitochondrial metabolism, and amyloid-β uptake in astrocytes

TL;DR: Results indicate that a reduction in IGF-1 receptor (IGFR) expression with age is associated with decline in hippocampal-dependent learning and increased gliosis, which may contribute to the pathogenesis of Alzheimer's disease and other age-associated cognitive pathologies.
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Hypoxia-inducible Factor 2α Regulates Expression of the Mitochondrial Aconitase Chaperone Protein Frataxin

TL;DR: The studies reveal that Fxn, like Sod2, is a nuclear-encoded, mitochondrial-localized HIF-2α target gene required for optimal mitochondrial homeostasis and expand upon the previously defined role of Hif-2 α in the cellular response to oxidative stress.
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Selective Inhibition of Deactivated Mitochondrial Complex I by Biguanides

TL;DR: In this article, the relative sensitivity of active/de-active complex I to biguanide-mediated inhibition and resulting superoxide radical (O₂(• )) production was determined.