Heart Killer Protein Identified

Researchers have managed to identify a protein kinase called ROCK-1 believed to be responsible for erectile dysfunction (ED), high blood pressure and heart failure. The discovery may ultimately allow doctors to remove ED, keep blood pressure under control and also stop heart failure before it starts.

According to researchers Dr. Robert Schwartz of the Texas A&M Health Science Center and Dr. Michael Schneider & Dr. Mark Entman from Baylor College of Medicine, both in Houston, their search for metabolic events crucial for development of heart failure led them to this discovery.

“Cell death in the heart is normally a very slow process,” Dr. Schwartz said. “It can take 40 years for a heart muscle cell to die and be replaced. In heart failure, that process goes to completion in eight months to two years, but that still gives us time to do something useful if we can find the right way to go about it.”

The researchers found presence of low levels of the activated form of an enzyme called caspase-3 in every heart failure patient. Almost all cardiologists keep caspase-3 under control through what is known as the “survival factor” – AKT. Closer observation revealed even small increases in levels of caspace-3 triggered a circular mechanism that speeded up cell death in the heart muscle. These small increases could be the result of high blood pressure, previous heart attacks, or other cardiac events.

“Activated caspase-3 chips pieces off ROCK-1, which is a protein kinase, in a special way” Dr. Schwartz explained. “One of these pieces turns on a gene called PTEN that stops the formation of Akt. When Akt is no longer inhibiting caspase-3 activity, it goes out of control and the process goes on and on until the heart muscle is destroyed.”

Therapeutically it is not possible to inhibit caspace-3 because it would also stop stem cell and blood cell production in the bone marrow. In the researchers’ opinion the best way to break the cycle is to find a drug capable of inhibiting ROCK-1. Such a drug would also have a dilatory effect on blood vessels thereby relieving hypertension and ED, both of which are results of contraction of blood vessels.

“Blood vessel dilation is the principle behind Viagra,” Dr. Schwartz explained. The research team bred a mouse free from ROCK-1 production to test the safety of their proposed intervention. The animal remained healthy in all aspects unless it developed a cardiac overload.

The researchers hypothesized this happened on account of ROCK-2, the back-up for ROCK-1 keeping all necessary ROCK functions like cell motion and smooth-muscle contractility going in ROCK-1’s absence. This despite the fact ROCK-2 does not take part in cardiac events.

Describing the new research as highly encouraging, Dr. Mandeep Mehra, Head of Cardiology at the University of Maryland School of Medicine said, “There’s a real need for new therapeutics in the treatment of heart failure. Current therapy focuses on inhibiting neurohormonal proteins that damage the heart and are responsible for the progression of the disease. When we stack new pharmacological treatments on top of each other to affect all of these hormones, we notice that, after a while, our treatment is no longer effective.”

At the same time, Dr. Mehra also cautioned the option of blocking the ROCK-1 – caspase-3 pathway was not being considered the first time. In his opinion the effects were short-lived. His main concern however was the effect of ROCK-1 inhibition on the development of cancer.

“Some cancer treatments work because they raise the level of ROCK-1,” Dr. Mehra said. “If ROCK-1 levels are lowered, it might accelerate the progression of existing cancers or encourage the growth of new ones, but this is speculation. We will have to wait until the drug is developed and tested to find out. It might not happen or there might be a way around this effect if it does.”

Disagreeing with Dr. Mehra views, Dr. Schwartz said, “Since ROCK-1 helps regulate cell motion, ROCK-1 inhibitors could cut down cancer’s metastatic spread, which might be a good therapeutic trade-off.”

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