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Particular Protein Fragments Mitochondria During Heart Attacks

At the time of a heart attack, the heart cells are deprived of oxygen which known as hypoxia. This low oxygen supply causes the mitochondria, the powerhouse, to break down bringing about cell impairing which is followed by heart failure. The entire processes stepwise details still remain unclear. At present, researchers from the National Institute for Physiological Sciences have publicized how filamin A, a vital factor of the cell skeleton, intermingles in the company of the protein Drp1 in hypoxic circumstances to assist mitochondrial fission.

The researchers have proved their research after through studying of mouse or rat models having heart attacks and analyzing the filamin A and Drp1’s actions in various conditions. The researchers have been able to find that the cilnidipine drug can aid in keeping this damaging process at bay. According to Motohiro Nishida, the cell skeleton’s vital factor helps Drp1 to bond to the mitochondria in the usual cases but when the oxygen supply is depleted then the Drp1 binding process is increased which is followed by fragmentation of the mitochondria. The detailed investigation using immunochemical methods, surgical procedures, and sub-cellular components analysis has helped determine that the hypoxic stress tends to activate the filamin A and Drp1 interaction and in turn boosts Drp1 activity which finally causes a heart attack.

The skeleton of the entire mechanism is still vague and requires more research before jumping into conclusions. However, the Drp1’s role in fragmentation of mitochondria has been confirmed by the current study. The drug cilnidipine is confirmed to save the heart cells from damage. This is a miracle drug as there are no other clinically applicable drugs that can control the mitochondrial fission progression in heart disease. This study can definitely help the future research aiming in curbing mitochondrial fission. A team of physicians, geneticists, and biologists from the University of Arizona have together found that the people with a unique genetic factor, rs17114036, tend to remain resistant to plaque formation and also have a low risk developing coronary artery disease.