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David R. Pimentel

Researcher at Boston University

Publications -  74
Citations -  9131

David R. Pimentel is an academic researcher from Boston University. The author has contributed to research in topics: Oxidative stress & Myocyte. The author has an hindex of 44, co-authored 72 publications receiving 8460 citations. Previous affiliations of David R. Pimentel include Boston Medical Center & Boston University Medical Campus.

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Adiponectin protects against myocardial ischemia-reperfusion injury through AMPK- and COX-2—dependent mechanisms

TL;DR: It is suggested that adiponectin protects the heart from ischemia-reperfusion injury through both AMPK- and COX-2–dependent mechanisms.
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Norepinephrine Stimulates Apoptosis in Adult Rat Ventricular Myocytes by Activation of the β-Adrenergic Pathway

TL;DR: NE, acting via the ss-adrenergic pathway, stimulates apoptosis in adult rat cardiac myocytes in vitro and requires calcium entry via voltage-dependent calcium channels, which may contribute to the progression of myocardial failure.
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Adiponectin-mediated modulation of hypertrophic signals in the heart.

TL;DR: It is found that pressure overload in adiponectin-deficient mice resulted in enhanced concentric cardiac hypertrophy and increased mortality that was associated with increased extracellular signal-regulatedKinase (ERK) and diminished AMP-activated protein kinase (AMPK) signaling in the myocardium.
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S-Glutathiolation by peroxynitrite activates SERCA during arterial relaxation by nitric oxide

TL;DR: In this paper, it was shown that NO-derived peroxynitrite (ONOO) directly increases SERCA activity by S-glutathiolation and that this modification of SERCA is blocked by irreversible oxidation of the relevant cysteine thiols during atherosclerosis.
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Role of Oxidative Stress in Myocardial Hypertrophy and Failure

TL;DR: Increasing evidence from experimental models of on the nuclear genome but localizes to mitochondria via a mitochondrial targeting sequence, heart failure supports the concept that there is increased oxidative stress in the failing heart, and makes up >70% of the SOD activity in the heart and >90% the activity in cardiac myocytes.