By Wilbert S. Aronow MD FACC FAHA FACP FCCP, John Arthur McClung MD FACP FACC FAHA FASE
Translational study in Coronary Artery ailment: Pathophysiology to therapy covers the complete spectrum of simple technology, genetics, drug therapy, and interventions for coronary artery affliction. With an emphasis on vascular biology, this reference absolutely explains the basic facets of coronary artery disorder pathophysiology.
Included are very important themes, together with endothelial functionality, endothelial damage, and endothelial fix in a variety of ailment states, vascular tender muscle functionality and its interplay with the endothelium, and the interrelationship among inflammatory biology and vascular functionality.
By supplying this synthesis of present study literature, this reference permits the cardiovascular scientist and practitioner to entry every little thing they want from one source.
- Provides a concise precis of modern advancements in coronary and vascular learn, together with formerly unpublished data
- Summarizes in-depth discussions of the pathobiology and novel therapy concepts for coronary artery disease
- Provides entry to an accompanying site that includes images and movies of noninvasive diagnostic modalities for evaluate of coronary artery affliction
Read Online or Download Translational research in coronary artery disease : pathophysiology to treatment PDF
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Extra info for Translational research in coronary artery disease : pathophysiology to treatment
Sample text
LOX-1 itself acts as a potent pro-oxidant and pro-inflammatory molecule. Sawamura’s group showed that LOX-1 antibody attenuated the inflammatory response to lipopolysaccharide in rats [6]. Mehta et al. [7,8] demonstrated that deletion of LOX-1 gene reduced atherosclerosis in LDLr null mice fed an atherogenic diet, confirming the role of LOX-1 in atherogenesis. LOX-1 is also upregulated in the heart following ischemia and reperfusion injury and is associated with markers of inflammation and oxidative stress.
Impaired pAMPK and pAkt signaling has been implicated in insulin resistance and endothelial dysfunction. HO-1 induction mediates activation of pAMPK and pAkt, increases glucose transport, fatty acid oxidation, mitochondrial function, and NO bioavailability, and improves vascular function [27–30]. Burgess et al. demonstrated that HO-1 induction in adipocyte stem cells not only ameliorates obesityassociated metabolic consequences, including hypertension independent of body weight, but also improves glucose tolerance in both male and female obese mice [31].
Selecting a patient population with low levels of vascular inflammation and inadequacies of imaging techniques are postulated as the reasons for the negative outcome. Larger studies that include appropriate patients with increased vascular inflammation, such as those with ACS, and improvement in imaging specificity can further our quest of an antibody against atherosclerosis. Vaccine Against Atherosclerosis The search of a vaccine that can protect against atherosclerosis would be considered the Holy Grail in the prevention of CAD.