A nitrozatív stressz szerepe a kardiovaszkuláris rendszer szabályozásában = Regulation of cardiovascular responses by nitrosative stress

Kimutattuk az oxidalt LDL eredetu 7-ketokoleszterin PARP aktivaciot okozo hatasat. Kkimutattuk hogy az endotoxemia altal kivaltott PARP aktivaciot inzulinnal gatolni lehet, vagyis a PARP aktivacio indirekt jelenseg, a hiperglikemia eredmenye. A PARP enzim szerepet kimutattuk thorakoabdominalis aorta okkluziot kovető reperfuzioban is. A PARP gatlok előnyos hatasait kimutattuk szivelegtelenseg es reperfuzios modellekben, es uj biokemiai valtozasokat irtunk le ezen folyamatok kapcsan. Kimutattuk a PARP aktivacio jelenletet periferias ver lekukocitain miokardialis infarktusban szenvedo betegekben. Kimutattuk, hogy human szivmitokondriumok nem termelnek relevans mennyisegben NO-t. Kimutattuk hogy szamos olyan gyogyszermolekula, amely direkt vagy indirekt modon gatolja a PARP enzimet, kardioprotektiv hatasu. Kimutattuk a PARP aktivacio szerepet egy eger kontakt hiperszenzitivitas modellben. Kimutattuk a protein kinaz C szerepet a PARP aktivacioban. Kimutattuk a nitrozativ stressz es PARP szerepet terhessegi diabeteszben. Kimutattunk egy uj mitokondrialis poliADPribozilacios reakcioutat. | We have demonstrated the ability of the oxidized LDL derived 7-ketocholesterol to induce PARP activation. We have demonstrated that endotoxin-induced PARP activation is the result of stress-hyperglycemia. We have demonstrated the role of PARP in the reperfusion injury associated with TAAA surgery. We have demonstrated the beneficial effects of PARP inhibitors in cardiac insufficiency and myocardial reperfusion models, and have demonstrated novel biochemical alterations associated with the PARP pathway. We have demonstrated the activation of PARP in circulating leukocytes from patients undergoing acute myocardial infarction. We have demonstrated that many drug molecules that are inhibiting PARP in a direct or indirect fashion exert cardioprotective effects in vitro. We have shown the role of PARP activation in a murine model of contact hypersensitivity. We have shown the role of PKC in the activation of PARP in vitro. We have shown the role of nitrosative stress and PARP activation in gestational diabetes in humans. We have described a new mitochondrial PARylation pathway.