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Matthew C. Zimmerman

Researcher at University of Nebraska Medical Center

Publications -  127
Citations -  5495

Matthew C. Zimmerman is an academic researcher from University of Nebraska Medical Center. The author has contributed to research in topics: Angiotensin II & Medicine. The author has an hindex of 35, co-authored 97 publications receiving 4594 citations. Previous affiliations of Matthew C. Zimmerman include University of California, San Francisco & Roy J. and Lucille A. Carver College of Medicine.

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A dynamic pathway for calcium-independent activation of CaMKII by methionine oxidation

TL;DR: It is shown that oxidation of paired regulatory domain methionine residues sustains CaMKII activity in the absence of Ca2+/CaM and highlights the critical importance of oxidation-dependent CaMK II activation to AngII and ischemic myocardial apoptosis.
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Hypertension Caused by Angiotensin II Infusion Involves Increased Superoxide Production in the Central Nervous System

TL;DR: The data suggest that increased intracellular O2·− production in the SFO is critical in the development of Ang II–induced hypertension, and Adenoviral-mediated delivery of cytoplasmically targeted superoxide dismutase (SOD) selectively to this site prevented the hypertension and the increased O2 ·− production.
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Superoxide Mediates the Actions of Angiotensin II in the Central Nervous System

TL;DR: A novel signaling mechanism mediating the actions of Ang II in the CNS is identified, and dysregulation of this signaling cascade may be important in hypertension and heart failure triggered by Ang II acting in the central nervous system.
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Induction of oxidative and nitrosative damage leads to cerebrovascular inflammation in an animal model of mild traumatic brain injury induced by primary blast.

TL;DR: The hypothesis that cerebral vascular injury occurs before the development of neurological disorders in mild TBI was confirmed by the activation of caspase-3 and cell apoptosis mostly around the perivascular region and induction of oxidative stress and activation of matrix metalloproteinases by shock wave underlie the mechanisms of cerebral vascular BBB leakage and neuroinflammation.
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Requirement for Rac1-Dependent NADPH Oxidase in the Cardiovascular and Dipsogenic Actions of Angiotensin II in the Brain

TL;DR: Results identify a Rac1-dependent NADPH oxidase as the source of central Ang II–induced O2·− production, and implicate this oxidase in cardiovascular diseases associated with dysregulation of brain Ang II signaling, including hypertension.