George Kunkel

George Kunkel
Stanford University School of Medicine · Medicine

PhD

About

14
Publications
2,681
Reads
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223
Citations
Additional affiliations
August 2018 - July 2019
Columbia University
Position
  • MPH Candidate
May 2018 - August 2018
Nashville State Technical Community College
Position
  • Professor (Associate)
August 2014 - August 2017
University of Louisville
Position
  • PhD Student

Publications

Publications (14)
Article
Hospital Dentistry is an inclusive synergism of the recognized dental specialties in an emergency/hospital atmosphere. This perspective composition serves to display the breadth of Hospital Dentistry from an observational and creative viewpoint while elucidating the role of the Hospital Dentist in the dynamic large university hospital setting. It c...
Article
Full-text available
Heart failure (HF) is a functional lack of myocardial performance due to a loss of molecular control over increases in calcium and ROS, resulting in proteolytic degradative advances and cardiac remodeling. Mitochondria are the molecular powerhouse of cells, shifting the sphere of cardiomyocyte stability and performance. Functional mitochondria rely...
Article
Full-text available
Although hyperhomocysteinemia (HHcy) is known to promote downstream pro-inflammatory cytokine elevation, the precise mechanism is still unknown. One of the possible receptors that could have significant attention in the field of hypertension is toll-like receptor 4 (TLR-4). TLR-4 is a cellular membrane protein that is ubiquitously expressed in all...
Article
Although mitochondrial transcription factor A (TFAM) is a protective component of mitochondrial DNA and a regulator of calcium and reactive oxygen species (ROS) production, the mechanism remains unclear. In heart failure (HF), TFAM is significantly decreased and cardiomyocyte instability ensues. TFAM inhibits Nuclear Factor of Activated T cells (NF...
Article
Full-text available
Skeletal muscle atrophy is the consequence of protein degradation exceeding protein synthesis. This arises for a multitude of reasons including the unloading of muscle during microgravity, post-surgery bedrest, immobilization of a limb after injury, and overall disuse of the musculature. The development of therapies prior to skeletal muscle atrophy...
Article
Full-text available
Mitochondrial dysfunction underlines a multitude of pathologies; however, studies are scarce that rescue the mitochondria for cellular resuscitation. Exploration into the protective role of mitochondrial transcription factor A (TFAM) and its mitochondrial functions respective to cardiomyocyte death are in need of further investigation. TFAM is a ge...
Article
Background: A significant number of studies have shown a positive correlation between Hcy plasma levels and hypertension. On the other hand pathogen recognition receptor, and in particular TLR-4 is a foreign antigen sensor that plays role in innate immune system activation and has recently gained a significant attention in the field of hypertension...
Article
Hyperhomocysteinemia (HHcy) has been observed to promote hypertension, but the mechanisms are unclear. Toll-like receptor 4 (TLR-4) is a cellular membrane protein that is ubiquitously expressed in all cell types of the vasculature. TLR-4 activation has been known to promote inflammation that has been associated with pathogenesis of hypertension. In...
Article
Although cardiac resuscitation can revive the whole body, the mechanisms are unclear. To this end, we propose that reviving a dead/dysfunctional cardiomyocyte will shed light on resuscitation mechanisms and pave the way to treat cardiac myopathies. The degradation of the myocyte cytoskeleton by the proteasome system which involves calpains, ubiquit...
Article
Full-text available
Mitochondrial dysfunction has been reported to underline heart failure, and our earlier report suggests that mitochondrial fusion and fission contributes significantly to volume overload heart failure. Although ample studies highlight mitochondrial dysfunction to be a major cause, studies are lacking to uncover the role of mitochondrial epigenetics...

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