Assistant Professor, Medicine, Boston University School of Medicine
Cardiology
Dr. David R. Pimentel, MD
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David R. Pimentel, MD practices Cardiology. He studied medicine at University of Maryland School of Medicine. University of Maryland School of Medicine has a rank of 37 in research and a 52 in primary care David Pimentel has written publications. He has 49 publications published with PubMed. The lastest publication is: 'Norepinephrine stimulates apoptosis in adult rat ventricular myocytes by activation of the beta-adrenergic pathway.' David Pimentel is registered with Medicare and accepts Medicare payments.
Publications
- High fat, high sucrose diet causes cardiac mitochondrial dysfunction due in part to oxidative post-translational modification of mitochondrial complex II.
- Non-invasive imaging for cardiac amyloidosis - Delaying the obvious?
- Adiponectin modulates oxidative stress-induced autophagy in cardiomyocytes.
- Activation of thromboxane receptor modulates interleukin-1β-induced monocyte adhesion--a novel role of Nox1.
- Cardiac myocyte follistatin-like 1 functions to attenuate hypertrophy following pressure overload.
- Mitochondrial transporter ATP binding cassette mitochondrial erythroid is a novel gene required for cardiac recovery after ischemia/reperfusion.
- Adiponectin mediates cardioprotection in oxidative stress-induced cardiac myocyte remodeling.
- Cardiac myocyte-specific ablation of follistatin-like 3 attenuates stress-induced Myocardial hypertrophy.
- Redox regulation of sirtuin-1 by S-glutathiolation.
- Cardiac-specific overexpression of catalase identifies hydrogen peroxide-dependent and -independent phases of Myocardial remodeling and prevents the progression to ove...
- Cardiac-specific deletion of LKB1 leads to hypertrophy and dysfunction.
- Activin A and follistatin-like 3 determine the susceptibility of Heart to ischemic injury.
- Fenofibrate inhibits aldosterone-induced apoptosis in adult rat ventricular myocytes via stress-activated kinase-dependent mechanisms.
- Palmitate alters neuregulin signaling and biology in cardiac myocytes.
- Follistatin-like 1 is an Akt-regulated cardioprotective factor that is secreted by the Heart.
- A novel mutant cardiac troponin C disrupts molecular motions critical for calcium binding affinity and cardiomyocyte contractility.
- Cysteine-674 of the sarco/endoplasmic reticulum calcium ATPase is required for the inhibition of cell migration by nitric oxide.
- Role of reversible, thioredoxin-sensitive oxidative protein modifications in cardiac myocytes.
- Oleate prevents palmitate-induced cytotoxic stress in cardiac myocytes.
- Adiponectin protects against Myocardial ischemia-reperfusion injury through AMPK- and COX-2-dependent mechanisms.
- A new hypertrophic mechanism of serotonin in cardiac myocytes: receptor-independent ROS generation.
- Alpha-adrenergic receptor-stimulated hypertrophy in adult rat ventricular myocytes is mediated via thioredoxin-1-sensitive oxidative modification of thiols on Ras.
- Adiponectin-mediated modulation of hypertrophic signals in the Heart.
- S-Glutathiolation by peroxynitrite activates SERCA during arterial relaxation by nitric oxide.
- Statins inhibit beta-adrenergic receptor-stimulated apoptosis in adult rat ventricular myocytes via a Rac1-dependent mechanism.
- S-glutathiolation of Ras mediates redox-sensitive signaling by angiotensin II in vascular smooth muscle cells.
- Angiotensin II differentially regulates interleukin-1-beta-inducible NO synthase (iNOS) and vascular cell adhesion molecule-1 (VCAM-1) expression: role of p38 MAPK.
- Human amyloidogenic light chains directly impair cardiomyocyte function through an increase in cellular oxidant stress.
- L-Homocysteine and L-homocystine stereospecifically induce endothelial nitric oxide synthase-dependent lipid peroxidation in endothelial cells.
- Temporal control of NF-kappaB activation by ERK differentially regulates interleukin-1beta-induced gene expression.
- Glucose-6-phosphate dehydrogenase modulates cytosolic redox status and contractile phenotype in adult cardiomyocytes.
- Beta-adrenergic receptor-stimulated apoptosis in cardiac myocytes is mediated by reactive oxygen species/c-Jun NH2-terminal kinase-dependent activation of the mitochon...
- Role of reactive oxygen species and NAD(P)H oxidase in alpha(1)-adrenoceptor signaling in adult rat cardiac myocytes.
- Adventitial delivery of dominant-negative p67phox attenuates neointimal hyperplasia of the rat Carotid artery.
- Association of mitochondrial antioxidant enzymes with mitochondrial DNA as integral nucleoid constituents.
- Regulation of cell physiology and pathology by protein s-glutathionylation: lessons learned from the cardiovascular system.
- S-glutathiolation of p21ras by peroxynitrite mediates endothelial insulin resistance caused by oxidized low-density lipoprotein.
- Activation of thromboxane receptor upregulates interleukin (IL)-1beta-induced VCAM-1 expression through JNK signaling.
- The FOXO3a transcription factor regulates cardiac myocyte size downstream of AKT signaling.
- Reactive oxygen species mediate amplitude-dependent hypertrophic and apoptotic responses to mechanical stretch in cardiac myocytes.
- Norepinephrine stimulates apoptosis in adult rat ventricular myocytes by activation of the beta-adrenergic pathway.
- Role of oxidative stress in myocardial hypertrophy and Failure.
- H(2)O(2) regulates cardiac myocyte phenotype via concentration-dependent activation of distinct kinase pathways.
- NADPH oxidase mediates angiotensin II-induced endothelin-1 expression in vascular adventitial fibroblasts.
- Strain-stimulated hypertrophy in cardiac myocytes is mediated by reactive oxygen species-dependent Ras S-glutathiolation.
- Cyclooxygenase-2 induction by adiponectin is regulated by a sphingosine kinase-1 dependent mechanism in cardiac myocytes.
- Adiponectin deficiency exacerbates cardiac dysfunction following pressure overload through disruption of an AMPK-dependent angiogenic response.
- High glucose oxidizes SERCA cysteine-674 and prevents inhibition by nitric oxide of smooth muscle cell migration.
Schools
University Of Maryland School Of Medicine
Boston Med Center
Procedures Preformed
- Ablation for Treatment of Cardiac Arrhythmias
- Cardiac Catheterization (incl. Coronary Angiography)
- Cardiac Imaging
- Cardiac MRI (Magnetic Resonance Imaging) of Heart or Chest
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Conditions Treated
- Angina and Acute Coronary Syndrome
- Aortic Aneurysm
- Aortic Dissection
- Aortic Valve Disease
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Doctors Specialties
- Cardiology
Accepted Insurances
- Blue Card PPO
- BlueConnect HMO
- Blue with Managed Care Behavioral Health HMO
- Preferred Blue PPO
- Cigna HMO
- Cigna PPO
- LocalPlus
- Open Access Plus
- Commercial Insurance Company
- First Health (Coventry Health Care) PPO
- Harvard Pilgrim Health Care PPO
- HealthFirst
- Humana
- Medicaid
- Medicare MCR
- MultiPlan PPO
- Neighborhood Health Plan
- Tufts Health Plans
- Tufts PPO
- Choice Plus POS
- United Healthcare
Education
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Boston University Medical Center -
University of Maryland School of Medicine
Hospital
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Boston Medical Center
Drug Facts
| NPI NUMBER | 1396722203 | |
| NPPES Provider LastName | PIMENTEL | |
| NPPES Provider FirstName | DAVID | |
| NPPES Provider ZIPCode | 021182309 | |
| NPPES Provider State | MA | |
| Specialty Description | Cardiology | |
| Total Claim Count | 2452.0 | |
| Distinct Opioid Count | 0.0 | |
| Opioid Claim Count | 0.0 | |
| Percent Opioid Claims | 0.0 |
Helpful Reviews
Medicare Facts
| National Provider Identifier [NPI] | 1396722203 |
| Last Name Of The Provider | PIMENTEL |
| First Name Of The Provider | DAVID |
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