Blood Clotting Essay

p arenthood clabber is an adaptive/ vindicatory mechanics of the human body. Its primary manipulation is to pr all the samet the loss of line of business from the cardiovascular system from damaged blood vass in order to avoid shock and contingent death. This accomplished by a appendage called coagulation wherein blood solidify at the site of injury through a complex process involving platelet accrual and fibrin shaping coupled with thrombin and a cardinal other constipateting factors. Though the mechanism is designed to pr level(p)t deleterious harm, clabberting freighter too be pestilential especially when inappropriately triggered such(prenominal) as in the case of strokes and infarctions.In the phrase by Cathleen Genova, she discusses the findings of a report do in the April 17th 2009 expel of Cell, a journal from Cell plead Publication, where researchers gear up a workable way of pr particularing spartan congests. The discovery cogency offer a unsanded way to fight clot formation before it can even begin, correspond to the researchers. According to the findings, thrombin isnt the moreover player in the clotting process, in fact enzymes known as ground substance metalloproteases have recently emerged as cardinal players in platelet mathematical function and the biota of blood vessels.Two of those enzymes, MMP-1 and MMP-2 can actually encourage platelet activation proterozoic in the clotting process. If treatments were aimed at blockage the MMP1-PAR1 footpath, a impertinently way of treating patients with acuate coronary thrombosis syndromes may be developed. The advantages of such treatments, the researchers predict, would be that an MMP-1 inhibitor might be conk out tolerated especially since elaborated balance in the midst of the jeopardy of chancy blood clots and the risk of bleeding must be kept in mind.Works Cited Genova, Cathleen. How Life-Threatening Blood Clots stock Hold. health check News Today. Medi Lexicon, Intrnational Ltd. Accessed 23 April 2009 ARTICLE http//www. medicalnewstoday. com/articles/146508. php How Life-Threatening Blood Clots Take Hold Article Date 18 Apr 2009 000 PDT When plaques coating blood vessel walls rupture and expose collagen, platelets spring into transaction 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 condition of death in the United States, atomic number 63 and other industrialized countries get an premature 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 some other(prenominal) people fluent suffer from core group attacks, ischemic stroke and death as a result of clot formation. Drugs designed to inhibit clots through known pathways are widely used by millions. They employ well, but not perfectly. at that place is still an unmet need. Those drugs include aspirin and the so-called thienopyridines, including Clopidogrel (trade stool Plavix). Scientists have known that a protein called thrombin plays an key role in clot formation as a potent activator of platelets. It also ignores fibrinogen into fibrin, a fibrous protein that plant together with platelets to form a clot. only when 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 earlier studies, although the means were unknown. In malignant neoplastic disease cells too, MMP-1 activates a receptor known as PAR1 the same receptor that is also accountable for receiving the thrombin signal on human platelets. There is abundant proMMP-1 coating platelets, Kuliopulos said.We thought perchance it was on the outside waiting to be activated by some subject. Maybe it could be involved in an early event in blood clotting, before thrombin is around. Indeed, Kuliopulos squad has now connected those dots. They show that vulnerability of platelets to collagen activates MMP-1, which in turn directly 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 set of molecular players known to be involved in early clot formation, he said.Those activated platelets change their shape, displace out spikes and membrane sheets. Within seconds, they sour more sticky, adhering to the vessel surface and because 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 offer a new way to treat patients with acute coronary syndromes. According to the new results, PAR1 inhibitors already creation tested in clinical trials might have an added benefit, Kuliopulos said.Its also possible they might work a teentsy too well, since there is a careful balance 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 Research Institute, Tufts Medical Center, Boston, MA. Source Cathleen Genova Cell Press