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Emma Yu
University of Cambridge
Mitochondrial DNAMitochondrionReactive oxygen speciesDiabetes mellitusMedicine
20Publications
9H-index
613Citations
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Publications 19
Newest
#1Alexander M. Reyzelman (Samuel Merritt University)H-Index: 16
Last. Ran MaH-Index: 1
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BACKGROUND: Over 30 million people in the United States (over 9%) have been diagnosed with diabetes. About 25% of people with diabetes will experience a diabetic foot ulcer (DFU) in their lifetime. Unresolved DFUs may lead to sepsis and are the leading cause of lower-limb amputations. DFU rates can be reduced by screening patients with diabetes to enable risk-based interventions. Skin temperature assessment has been shown to reduce the risk of foot ulceration. While several tools have been devel...
9 CitationsSource
#1Emma Yu (University of Cambridge)H-Index: 9
#2Kirsty Foote (University of Cambridge)H-Index: 5
Last. Martin R. Bennett (University of Cambridge)H-Index: 68
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4 CitationsSource
#1Kirsty Foote (University of Cambridge)H-Index: 5
#2Johannes Reinhold (University of Cambridge)H-Index: 9
Last. Martin R. Bennett (University of Cambridge)H-Index: 68
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: Aging is the largest risk factor for cardiovascular disease, yet the molecular mechanisms underlying vascular aging remain unclear. Mitochondrial DNA (mtDNA) damage is linked to aging, but whether mtDNA damage or mitochondrial dysfunction is present and directly promotes vascular aging is unknown. Furthermore, mechanistic studies in mice are severely hampered by long study times and lack of sensitive, repeatable and reproducible parameters of arterial aging at standardized early time points. W...
21 CitationsSource
Objective— Mitochondrial DNA (mtDNA) damage is present in murine and human atherosclerotic plaques. However, whether endogenous levels of mtDNA damage are sufficient to cause mitochondrial dysfunction and whether decreasing mtDNA damage and improving mitochondrial respiration affects plaque burden or composition are unclear. We examined mitochondrial respiration in human atherosclerotic plaques and whether augmenting mitochondrial respiration affects atherogenesis. Approach and Results— Human at...
36 CitationsSource
#1Jason M. Tarkin (University of Cambridge)H-Index: 13
#2Francis R. JoshiH-Index: 12
Last. James H.F. Rudd (University of Cambridge)H-Index: 45
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Background Inflammation drives atherosclerotic plaque rupture underlying most clinical events. While inflammation can be measured using 18F-fluorodeoxyglucose (FDG) positron emission tomography (PET), 18F-FDG lacks cell-specificity and is unreliable for coronary imaging owing to myocardial signal spillover. Up-regulation of somatostatin receptor-2 (SST2) occurs in activated macrophages offering a novel inflammation imaging target. Methods We comprehensively evaluated 68Ga-DOTATATE, a SST2 PET li...
Source
#1Jason M. Tarkin (University of Cambridge)H-Index: 13
#2Francis R. JoshiH-Index: 12
Last. James H.F. Rudd (University of Cambridge)H-Index: 45
view all 26 authors...
Abstract Background Inflammation drives atherosclerotic plaque rupture. Although inflammation can be measured using fluorine-18-labeled fluorodeoxyglucose positron emission tomography ([ 18 F]FDG PET), [ 18 F]FDG lacks cell specificity, and coronary imaging is unreliable because of myocardial spillover. Objectives This study tested the efficacy of gallium-68-labeled DOTATATE ( 68 Ga-DOTATATE), a somatostatin receptor subtype-2 (SST 2 )-binding PET tracer, for imaging atherosclerotic inflammation...
124 CitationsSource
#1Jason M. Tarkin (University of Cambridge)H-Index: 13
#2Francis R. JoshiH-Index: 12
Last. James H.F. Rudd (University of Cambridge)H-Index: 45
view all 26 authors...
Introduction: Activated macrophages express somatostatin receptor subtype-2 (SST2) within unstable and high-risk atherosclerotic plaques. Hypothesis: We tested the hypothesis that 68Ga-DOTATATE, a clinical SST2 PET tracer, is a more specific macrophage marker than 18F-FDG, and is superior for coronary imaging. Methods: In this prospective clinical study, 42 patients with stable or unstable atherosclerosis underwent 68Ga-DOTATATE and 18F-FDG PET imaging of carotid, aorta and coronary arteries. PE...
#1Emma Yu (University of Cambridge)H-Index: 9
#2Martin R. Bennett (University of Cambridge)H-Index: 68
Abstract Mitochondria are the cellular powerhouses, fuelling metabolic processes through their generation of ATP. However we now recognise that these organelles also have pivotal roles in producing reactive oxygen species (ROS) and in regulating cell death, inflammation and metabolism. Mitochondrial dysfunction therefore leads to oxidative stress, cell death, metabolic dysfunction and inflammation, which can all promote atherosclerosis. Recent evidence indicates that mitochondrial DNA (mtDNA) da...
32 CitationsSource
#1Emma Yu (University of Cambridge)H-Index: 9
#2Martin R. Bennett (University of Cambridge)H-Index: 68
Mitochondria are often regarded as the cellular powerhouses through their ability to generate ATP, the universal fuel for metabolic processes. However, in recent years mitochondria have been recognised as critical regulators of cell death, inflammation, metabolism, and the generation of reactive oxygen species (ROS). Thus, mitochondrial dysfunction directly promotes cell death, inflammation, and oxidative stress and alters metabolism. These are key processes in atherosclerosis and there is now e...
56 CitationsSource
#1Emma Yu (University of Cambridge)H-Index: 9
Introduction Mitochondrial DNA (mtDNA) damage occurs in both the vessel wall and in circulating cells in human atherosclerosis. However, whether mtDNA damage promotes atherogenesis or is a consequence of tissue damage is unknown. We assessed the hypothesis that mtDNA damage is present, and can directly promote atherosclerosis and affect plaque composition. Methods To assess whether mtDNA damage may contribute to atherogenesis we examined apolipoprotein E null mice (ApoE -/- ). We characterised t...
1 CitationsSource
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