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Cardiovascular Pathobiology
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CARing for pulminary arterial hypertension
Dr. Masa Komatsu's laboratory recently discovered a peptide that selectively targets and penetrates lung blood vessels affected by pulmonary arterial hypertension.
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The couch potato effect
The Kelly lab studies normal weight mice that don’t have the energy to exercise to better understand mitochondrial function in obesity and diabetes.
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The many flavors of diabetic heart disease
The diabetic heart is different from the non-diabetic failing heart in that it is filled with fat.
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Studying cardiovascular pathobiology
The Cardiovascular Pathobiology Program conducts research on fundamental and early translational aspects of cardiovascular biology, physiology, and disease. The predominant factors that contribute to cardiovascular diseases can be difficult to distinguish in a given individual because the heart and vasculature respond with a set of interrelated effects. For example, hypertension, ischemic injury, and diabetes all lead to pathologic cardiac remodeling that involves myocyte hypertrophy, fibrosis, and progressive ventricular dilatation. Similarly, hypertension, smoking, hypercholesterolemia, and diabetes lead to atherosclerosis. This is especially true in the obese or diabetic patient, given that hypertension and ischemic heart disease often coexist with inciting metabolic disturbances.
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Cardiovascular Pathobiology Program scientists focus on the pathobiological processes related to derangements of the obese and diabetic state, as well as other cardiovascular pathologic processes. This provides an opportunity to compare and contrast pathogenic mechanisms across disease etiologies. The Program is supported by a variety of specialized core technology platforms, including animal cardiometabolic phenotyping, ultra-high throughput small molecule screening in the Conrad Prebys Center for Chemical Genomics, and metabolomics. Scientists conduct research relevant to the following broad goals:
- Mechanisms of Disease - Delineation of etiology-specific mechanisms involved in the development of myocardial disease. Similar discovery-based studies focus on vascular disease, including atherosclerosis and hypertension.
- Biomarkers - Fundamental studies of mechanism to identify biochemical, genetic, or imaging-based biomarkers that define specific cardiovascular disease phenotypes in humans.
- Therapeutic Targets - Mechanistic studies combined with genomic/metabolite profiling show promise for the identification of candidate molecules and pathway targets for new therapies aimed at the early stages of disease and individualized by cardiovascular disease phenotype.
How our research helps improve health
In order to treat emerging heart and vascular diseases at the earliest stages, when disease-specific intervention is most likely to be effective, the underlying primary pathogenic mechanisms must be understood and well-defined. Otherwise, we are limited to the current array of therapies that are only partially effective. There are many "flavors" of heart failure that can result from a heart attack, high blood pressure, diabetes, or some other as-yet unidentified cause. Researchers are finding that the molecular mechanisms leading to various types of heart disease are different. Clearly defining each distinct pathway to heart failure will contribute to the development of new therapies tailored to the specific cause.
Research - Diabetes and Obesity - Cardiovascular Pathobiology: How
Our Research Helps |
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Research - Diabetes and Obesity - Cardiovascular Pathobiology: Recent
Developments
Recent Developments
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A Different Path to Fat-Related Heart Disease
Obesity and high-fat diets are major risk factors for lipotoxic cardiomyopathy, a condition where fat accumulates in heart cells. Dr. Rolf Bodmer and colleagues recently discovered an alternative cause – an imbalance in the fats that normally make up the basic structure of our cells- by studying an unusual model, the Drosophila fruit fly.
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Total skeletal muscle PGC-1 deficiency uncouples mitochondrial derangements from fiber type determination and insulin sensitivity.
Zechner C, Lai L, Zechner JF, Geng T, Yan Z, Rumsey JW, Collia D, Chen Z, Wozniak DF, Leone TC, Kelly DP.
Cell Metab. 2010 Dec 1;12(6):633-42.
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Peptide-directed highly selective targeting of pulmonary arterial hypertension.
Urakami T, Järvinen TA, Toba M, Sawada J, Ambalavanan N, Mann D, McMurtry I, Oka M, Ruoslahti E, Komatsu M.
Am J Pathol. 2011 Jun;178(6):2489-95. Epub 2011 May 6.
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Cardiovascular drug discovery in the academic setting: building infrastructure, harnessing strengths, and seeking synergies.
Gardell SJ, Roth GP, Kelly DP.
J Cardiovasc Transl Res. 2010 Oct;3(5):431-7. Epub 2010 Jul 13.
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Lipidomics at the interface of structure and function in systems biology.
Gross RW, Han X.
Chem Biol. 2011 Mar 25;18(3):284-91.
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Phospholipid homeostasis regulates lipid metabolism and cardiac function through SREBP signaling in Drosophila.
Lim HY, Wang W, Wessells RJ, Ocorr K, Bodmer R.
Genes Dev. 2011 Jan 15;25(2):189-200.
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Characterization of a novel angiogenic model based on stable, fluorescently labelled endothelial cell lines amenable to scale-up for high content screening.
Prigozhina NL, Heisel A, Wei K, Noberini R, Hunter EA, Calzolari D, Seldeen JR, Pasquale EB, Ruiz-Lozano P, Mercola M, Price JH.
Biol Cell. 2011 Oct 1;103(10):467-81.
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Research - Diabetes and Obesity - Cardiovascular Pathobiology:
Recent Publications |
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