Blood Clotting Essay

Blood clog upting is an adaptive/defensive utensil of the pitying body. Its primary purpose is to observe the loss of argumentation from the cardiovascular governance from damaged demarcation vessels in order to avoid shock and possible death. This accomplished by a process called coagulation wherein blood solidify at the site of deformity through a complex process involving blood platelet aggregation and fibrin establishment coupled with thrombin and a dozen other clotting factors. Though the mechanism is designed to prevent deleterious harm, clotting can also be harmful especially when inappropriately triggered much(prenominal) as in the berth of accidents and infarctions.In the article by Cathleen Genova, she discusses the findings of a motif made in the April 17th 2009 issue of Cell, a journal from Cell military press Publication, where researchers rig a possible way of preventing life-threatening clots. The discovery superpower wisecrack a new way to fight c lot system to begin with it can even begin, according to the researchers. According to the findings, thrombin isnt the only pseudo in the clotting process, in fact enzymes known as matrix metalloproteases have deep emerged as important players in platelet serve well and the biology of blood vessels.Two of those enzymes, MMP-1 and MMP-2 can actually encourage platelet activation early in the clotting process. If treatments were aimed at blocking the MMP1-PAR1 pathway, a new way of treating patients with acute coronary thrombosis syndromes may be developed. The advantages of such treatments, the researchers predict, would be that an MMP-1 oppressor might be better tolerated especially since careful parallelism between the risk of dangerous blood clots and the risk of bleeding mustiness be kept in mind.Works Cited Genova, Cathleen. How Life-Threatening Blood Clots defy Hold. Medical News Today. MediLexicon, Intrnational Ltd. Accessed 23 April 2009 <http//www. medicalnewst o-day. com/articles/146508. php> ARTICLE http//www. medicalnewstoday. com/articles/146508. php How Life-Threatening Blood Clots deem Hold Article Date 18 Apr 2009 000 PDT When plaques coating blood vessel walls rupture and expose collagen, platelets spring into action to form a blood clot at the damaged site.Now, a new report in the April 17th issue of the journal Cell, a Cell Press publication, reveals how those life-threatening clots a leading cause of death in the fall in States, Europe and other industrialized countries get an early grip. The discovery might offer a new way to fight clot formation before it can even begin, according to the researchers. Compared to other diseases, blood clotting has been very well understood, said Athan Kuliopulos of Tufts Medical Center and Tufts University School of Medicine.Nevertheless, he continued, many people still suffer from heart attacks, ischemic stroke and death as a result of clot formation. Drugs designed to inhibit clots thr ough known pathways are widely used by millions. They meet well, but not perfectly. There is still an unmet need. Those drugs include aspirin and the questionable thienopyridines, including Clopidogrel (trade name Plavix). Scientists have known that a protein called thrombin plays an important role in clot formation as a potent activator of platelets. It also cuts factor I into fibrin, a fibrous protein that practices together with platelets to form a clot. exclusively thrombin isnt the whole story. Enzymes known as matrix metalloproteases have recently emerged as important players in platelet function and the biology of blood vessels. Two of those enzymes, MMP-1 and MMP-2 can actually encourage platelet activation, according to precedent studies, although the means were unknown. In cancer cells too, MMP-1 activates a receptor known as PAR1 the same receptor that is also responsible for receiving the thrombin signal on human platelets. There is abundant proMMP-1 coating platel ets, Kuliopulos said.We thought maybe it was on the distant waiting to be activated by something. Maybe it could be baffling in an early event in blood clotting, before thrombin is around. Indeed, Kuliopulos aggroup has now connected those dots. They set up that exposure of platelets to collagen activates MMP-1, which in turn straight cut PAR1 on the surface of platelets. Collagen is the first thing a platelet sees when a blood vessel ruptures or is cut. The MMP-1-PAR1 pathway activates another make of molecular players known to be involved in early clot formation, he said.Those activated platelets change their shape, sending out spikes and membrane sheets. in spite of appearance seconds, they become more sticky, adhering to the vessel surface and then other platelets. Moreover, they show that treatments that block the MMP1-PAR1 pathway prevent blood clots from forming in the presence of collagen, suggesting that drugs targeting this metalloprotease-receptor system could off er a new way to treat patients with acute coronary syndromes. According to the new results, PAR1 inhibitors already being tested in clinical trials might have an added benefit, Kuliopulos said.Its also possible they might work a little too well, since there is a careful quietus between the risk of dangerous blood clots and the risk of bleeding. An MMP-1 inhibitor might be better tolerated, he said. The researchers include Vishal Trivedi, Adrienne Boire, Boris Tchernychev, Nicole C. Kaneider, Andrew J. Leger, Katie OCallaghan, Lidija Covic, and Athan Kuliopulos, of Tufts University School of Medicine, Molecular Oncology explore Institute, Tufts Medical Center, Boston, MA. Source Cathleen Genova Cell Press