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Specific type of cell death may accelerate decompensated heart failure

Autophagy, a normal process by which cells eat their own proteins to provide needed resources to the body in times of stress, may paradoxically cause harm to hearts already weakened by disease, researchers from UT Southwestern Medical Center have found.

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Keywords: specific, type, cell, death, accelerate, decompensated, heart, failure

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1. Specific type of cell death may accelerate decompensated heart failure
   07-05-2007 · UT Southwestern Medical Center
   Autophagy, a normal process by which cells eat their own proteins to provide needed resources to the body in times of stress, may paradoxically cause harm to hearts already weakened by disease, researchers from UT Southwestern Medical Center have found.
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2. JCI table of contents: January 2, 2007
   01-02-2007 · EurekAlert!
   This release contains summaries, links to PDFs and contact information for the following newsworthy papers to be published January 2, 2007, in the JCI, including: Genetic mutation alters response to heart failure drugs; Glucose levels trigger compensation for type 2 diabetics; Cell relocation fixes damage to the gut lining; BCL2 reins in BIM, preventing leukemic cell death; and Complex macrophage and monocyte interactions at work in atherosclerosis.
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3. Glycemic control medication appears to have favorable effect regarding risk of cardiovascular events
   09-11-2007 · EurekAlert!
   A meta-analysis of previous research suggests that use of pioglitazone -- a glycemic control medication for patients with type 2 diabetes -- significantly reduces the risk of heart attack, stroke and death, but increases the risk for serious heart failure, according to an article in the Sept. 12 issue of JAMA.
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4. Advance in understanding of blood pressure gene could lead to new treatments
   02-04-2007 · EurekAlert!
   Research by scientists at UCL (University College London) has clearly demonstrated for the first time the structure and function of a gene crucial to the regulation of blood pressure. The discovery could be important in the search for new treatments for illnesses such as heart disease, the UK's biggest killer. In a paper published online today in Nature Medicine, the team, led by Professor Patrick Vallance and Dr James Leiper, UCL Department of Medicine, reveal the role of the human gene dimethylarginine dimethylaminohydrolase (DDAH), showing that loss of DDAH activity disrupts nitric oxide (NO) production. NO is critical in the regulation of blood pressure, nervous system functions and the immune system. The role of DDAH is to break down modified amino acids (Asymmetric dimethylarginine (ADMA) and monomethyl arginine (L-NMMA)) that are produced by the body and have been shown to inhibit NO synthase. These molecules accumulate in various disease states including diabetes, renal failure and pulmonary and systemic hypertension, and their concentration in plasma (the fluid component of blood) is strongly predicative of cardiovascular disease and death. In a healthy human body, the majority of ADMA is eliminated through active metabolism by DDAH. Scientists have hypothesised that if DDAH function is impaired, NO production is reduced, and that this could be an important feature of increased cardiovascular risk. To examine this pathway in more detail, the researchers deleted the DDAH gene in mice. These mice went on to develop hypertension, or high blood pressure. They also designed specific inhibitors (small molecules) which bind to the active site of human DDAH. These small molecule inhibitors also induced hypertension in mice, confirming the importance of DDAH in the regulation of blood pressure. Dr Leiper, UCL Medicine, said: “These genetic and chemical approaches to disrupt DDAH showed remarkably consistent results, and provide compelling evidence that loss of DDAH function increases the concentration of ADMA and thereby disrupts vascular NO signalling. “There has been considerable scientific interest in this pathway and the role of ADMA as a novel risk factor, but so far there's been little evidence to support the idea that it's a cause of disease, rather than just a marker. Genes and their pathways are crucial to our understanding of cardiovascular disease and a better understanding of DDAH-1 could lead to important new treatments. “It could help us to establish if genetic variation predisposes certain people to these diseases, or whether environmental factors exert some of their effects through modulation of DDAH activity. “Our research also shows that this pathway could be harnessed therapeutically to limit production of NO in certain situations where too much nitric oxide is a bad thing; for example, hypotension and septic shock. These are some of the biggest problems in intensive care medicine and there is a huge unmet need for drug treatments.” The study, which was carried out at UCL's Rayne Institute, was funded by grants from the British Heart Foundation, the Wellcome Trust and the Medical Research Council. Professor Jeremy Pearson, Associate Medical Director of the British Heart Foundation, said: "The unexpected finding in the 1980s that a simple gas, nitric oxide (NO), is made by cells in the blood vessel wall and is a powerful control of blood vessel relaxation led to the award of the Nobel Prize in 1998 to its discoverers. "More recently, there has been increasing evidence that impairment of NO production is likely to be an important factor in the development of heart and circulatory disease, but the mechanisms responsible are not fully understood. "This study suggests for the first time that the loss of the activity of the enzyme DDAH-1 leads to reduced NO production and may cause heart and circulatory disease. These findings are likely to be important in the search for new ways to optimise the health of our blood vessels." ### Notes for Editors 1. For more information, please contact Ruth Metcalfe in the UCL Media Relations Office on tel: +44 (0)20 7679 9739, mobile: +44 (0)7990 675 947, out of hours: +44 (0)7917 271 364, e-mail: r.metcalfe@ucl.ac.uk2. 'Disruption of methylarginine metabolism impairs vascular homeostasis' is published in the February issue of the journal Nature Medicine. Advance online publication is embargoed to 18.00 GMT (13.00 US Eastern) Sunday 4 February 2007. Journalists can obtain copies of the paper by contacting the UCL Media Relations Office.3. The study was funded by the British Heart Foundation, the Wellcome Trust and the Medical Research Council. About UCL Founded in 1826, UCL was the first English university established after Oxford and Cambridge, the first to admit students regardless of race, class, religion or gender, and the first to provide systematic teaching of law, architecture and medicine. In the government's most recent Research Assessment Exercise, 59 UCL departments achieved top ratings of 5* and 5, indicating research quality of international excellence. UCL is the fourth-ranked UK university in the 2006 league table of the top 500 world universities produced by the Shanghai Jiao Tong University. UCL alumni include Mahatma Gandhi (Laws 1889, Indian political and spiritual leader); Jonathan Dimbleby (Philosophy 1969, writer and television presenter); Junichiro Koizumi (Economics 1969, Prime Minister of Japan); Lord Woolf (Laws 1954, Lord Chief Justice of England & Wales); Alexander Graham Bell (Phonetics 1860s, inventor of the telephone), and members of the band Coldplay.
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5. Pregnancy-related heart failure explained, symptoms reversed by simple hormone blocker
   02-08-2007 · EurekAlert!
   A new study reveals the mechanism responsible for a rare but potentially devastating form of heart failure that sometimes afflicts women late in pregnancy or shortly following childbirth, researchers have reported in the Feb. 9, 2007, issue of Cell, a publication of Cell Press. The so-called postpartum cardiomyopathy (PPCM) -- which is estimated to complicate one in every 1,300 to 4,000 deliveries in the US -- is considered among the leading causes of death among postpartum women in industrialized countries.
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6. JCI table of contents: Aug. 9, 2007
   08-09-2007 · EurekAlert!
   This release contains summaries, links to PDFs and contact information for the following newsworthy papers to be published online, Aug. 9, 2007, in the JCI, including: "New molecular regulators of hyperthyroidism and goiter"; "Cell death by necrosis leads to heart failure"; "Extent of apoptotic cell death affects risk factor for heart failure"; "New SNP for acute myeloid leukemia"; and "Battle of the bulge: what controls how much we eat."
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7. Novel candidate biomarker for heart failure also strongly predicts risk of death
   08-06-2007 · EurekAlert!
   A potential new biomarker for heart failure may be more powerful than established measures in identifying patients at increased risk for death from several causes. In their report, an international research team describes finding that blood levels of a protein called ST2 both indicate the presence of heart failure among patient with shortness of breath and powerfully predict the risk that a patient will die during the following year.
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8. Long-term use of diabetes drug increases heart attack risk by more than 40 percent
   09-11-2007 · EurekAlert!
   An analysis of four studies involving more than 14,000 patients found that long-term use of the diabetes drug rosiglitazone (Avandia) increased the risk of heart attack by 42 percent and doubled the risk of heart failure, according to a new report from researchers at Wake Forest University School of Medicine and colleagues. There was no effect on death from cardiovascular causes.
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9. Fetal heart-cell enzyme important in onset of heart failure
   02-18-2007 · EurekAlert!
   In almost all forms of heart failure, the heart begins to express genes that are normally only expressed in the fetal heart. Researchers have known for years that this fetal-gene reactivation happens, yet not what regulates it. Now, investigators at the Penn have discovered that an enzyme important in fetal heart-cell development regulates the enlargement of heart cells, known as cardiac hypertrophy, which is a precursor to many forms of congestive heart failure.
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10. Higher death rate for heart attack patients with additional non-cardiac conditions
    11-10-2006 · EurekAlert!
    Heart attack patients who also have another acute condition such as stroke, kidney failure and pneumonia may have a poorer outcome than those without these conditions, and those with the most severe conditions account for a disproportionate percentage of hospital deaths, researchers at Yale School of Medicine report in a recent American Journal of Medicine.
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