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Atrogin breaks down the side effects of statins

11-08-2007 · EurekAlert!

Statins are a popular class of drugs used to successfully combat high cholesterol. However, the rare, but serious, and poorly understood side effect of skeletal muscle breakdown prevents more prevalent use of these drugs. New research in mice has now indicated that atrogin-1 is a critical mediator of statin-induced muscle damage and that inhibiting atrogin-1 function might protect against this unwanted side effect of statins.

Keywords: atrogin, breaks, down, side, effects, statins, break, effect, statin

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JCI table of contents: Nov. 8, 2007
11-08-2007 · EurekAlert!
This release contains summaries, links to PDFs and contact information for the following newsworthy papers to be published online, Nov. 8, 2007, in the JCI, including: Atrogin breaks down the side effects of statins; Sex, sugar, and metabolic disease; New mouse strain teaches us about GPCRs; Too many red blood cells spoil the mouse; Two faces for TNF-alpha in antiviral and antitumor immunity; Making mice breathe easy: a role for IL-1 in lung damage; and others.
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Scientists identify gene responsible for statin-induced muscle pain
11-27-2007 · EurekAlert!
Statins, the popular class of drugs used to lower cholesterol, are among the most commonly prescribed medications in developed countries. But for some patients, accompanying side effects of muscle weakness and pain become chronic problems and, in rare cases, can escalate to debilitating and even life-threatening damage. Now a study led by investigators at Beth Israel Deaconess Medical Center, helps explain the source of these problems.
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Pine tree bark reduces side effects in hypertensive patients
11-15-2006 · EurekAlert!
A study published in the October journal of Clinical and Applied Thrombosis/Hemostasis shows Pycnogenol (pic-noj-en-all), an antioxidant plant extract from the bark of the French maritime pine tree reduced edema, a typical side effect of antihypertensive medications, by 36 percent in patients taking these medications.
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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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Study shows risk of acute pancreatitis low with statins
12-28-2006 · EurekAlert!
New research reveals that while cholesterol-lowering drugs do increase the risk of painful inflammation of the pancreas, the side effect is relatively rare, according to Sonal Singh, M.D., from Wake Forest University School of Medicine, and colleagues.
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Built-in molecular brakes curb the sniffles
01-17-2007 · EurekAlert!
Researchers at Johns Hopkins have discovered how our anti-infection machinery turns itself down and limits the sniffles, congestion and fevers that are a side effect of the campaign against invading viruses. The discovery seems to solve part of the mystery of why the misery of the common cold lasts only so long.
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New study shows Rescue Remedy is an effective all-natural stress, anxiety reliever
06-28-2007 · EurekAlert!
A just published scientific study conducted by researchers at the University of Miami School of Nursing in conjunction with The Sirkin Creative Living Center (SCLC) has found that Rescue Remedy, an all-natural remedy created from flower essences, is an effective over-the-counter stress reliever with a comparable effect to traditional pharmaceutical drugs yet without any of the known adverse side effects, including addiction.
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Carbon monoxide counteracts one side-effect of an anti-cancer drug
11-21-2007 · EurekAlert!
Doxorubicin (DOX) is a red-colored anti-cancer drug that carries serious side effects for the heart. These cardio-toxic effects are due to inhibition by DOX of mitochondrial biogenesis, a term used to describe cellular energy generation. In a new study, it is now shown that mitochondrial biogenesis can be recovered in DOX-treated rodents by either inhalation of carbon monoxide or overexpression of the protein HO-1.
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Story ideas from the Journal of Biological Chemistry
01-14-2008 · EurekAlert!
COX-2 inhibitors like Celecoxib have come under scrutiny lately due to adverse cardiovascular side-effects stemming from COX-2 reduction. In both fruit fly and rat models, researchers reveal another adverse effect of Celecoxib; this drug can induce arrhythmia. More interestingly, this effect is independent of the COX-2 enzyme.
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Provectus Pharmaceuticals, Inc. releases summary results of phase 1 metastatic melanoma study
09-18-2007 · EurekAlert!
Provecta demonstrated minimal side effects, significant efficacy and bystander effect on melanoma tumors in stage III patients.
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