Heart attack

Major breakthrough for heart diseases, organ transplants

Scientists at the Flanders Institute for Biotechnology (VIB) connected to the Katholieke Universiteit Leuven, while working on mice, have been able prevent muscle tissues from dying due to lack of oxygen. The breakthrough, they say, may hold implications in organ transplants and cardiovascular diseases.

Washington, Jan 7 : Scientists at the Flanders Institute for Biotechnology (VIB) connected to the Katholieke Universiteit Leuven, while working on mice, have been able prevent muscle tissues from dying due to lack of oxygen. The breakthrough, they say, may hold implications in organ transplants and cardiovascular diseases.

Normally, clogging of blood vessels results in a localized deficiency of oxygen that in turn causes the surrounding tissue to die. However, the new discovery may allow the muscle to 'adapt' to the lack of oxygen, an inherent metabolic mechanism in hibernating animals.

The study led by Peter Carmeliet, found that the oxygen meter PHD1, played a crucial role in this process.

Oxygen is vital to living beings, but it can also pose harm when it gets transformed into toxic oxygen particles causing grave damage to tissues and organs. Still, some animals like birds at high attitudes and hibernating animals turn down some body processes to utilize less oxygen in their body.

However, these changes in the amount of oxygen can be detected with certain sensors. These oxygen meters are vital in adapting the body's metabolism during the changeover from an oxygen-rich to an oxygen-deficient environment.

In the study, the researchers studied the role of PHD1 oxygen meter by using 'knock-out' mice that could not produce PHD1.

When an artery in these mice was blocked, thereby obstructing the oxygen supply to the muscle, it did not cause the death of the surrounding muscular tissue. This was a surprising result as the muscle received too little oxygen to survive under normal circumstances.

However, in the mice lacking the PHD1 oxygen meter, the tissue actually 'reprogrammed' itself through a metabolic shift, leading to the muscle needing less oxygen to continue functioning.

Now, less oxygen in the muscle implies fewer toxic oxygen particles and hence less damage. Thus, the little oxygen that was available could be used by the muscle in a better and safer manner.

These modifications allowed the muscle to stay perfectly healthy in these normally critical conditions.

Also, the researchers showed that if healthy mice are treated even briefly with a PHD1-blocker, it could protect the muscles against oxygen deficiency opening a path to new therapies.

These findings have significant implications for several medical applications, as further investigation may give knowledge about PHD1-blockers' mechanism in preventing blockage of blood vessels in heart attacks.

This may also lead to treatments for strokes and therapies by which surgeons are able to reduce the oxygen supply to organs for a longer period of time during many types of operations.

The absence of PHD1 might also explain the mysterious adaptations of hibernating animals, with important implications for the preservation of organs for transplant.

ANI