Clinical trials

The primary research objective of the project is to determine the role of eGC in microvascular reactivity in patients with coronary heart disease (CHD) before and after bypass grafting (cross-sectional study 2).The main objective of the project is to increase the excellence and interdisciplinarity of scientific work at MEFOS by connecting researchers from different scientific fields, improving conditions and resources for scientific work, and increasing international cooperation, in line with strategic objective 1: raising scientific excellence. The results of the project could provide pathophysiological insight into the development and maintenance of endothelial dysfunction in CVD, as well as identify new biomarkers for CVD.

The primary research objective of the project is to determine the role of eGC in microvascular reactivity in CKD (cross-sectional study 1). The main objective of the project is to increase the excellence and interdisciplinarity of scientific work at MEFOS by connecting researchers from different scientific fields, improving conditions and resources for scientific work, and increasing international cooperation, in line with strategic objective 1: raising scientific excellence. The results of the project could provide pathophysiological insight into the development and maintenance of endothelial dysfunction in CKD, as well as identify new biomarkers for CKD.

In the frame of this proposal investigators will test the hypothesis that high normal blood pressure (prehypertension; PreHT) induces systemic endothelial dysfunction and endothelial activation in both micro- and macrocirculation, reduces re-endothelialization potential of human endothelial progenitor cells (EPCs) and increases the level of endothelial extracellular vesicles (EVs), which are accompanied by increased oxidative stress level. Furthermore, initial vascular and left ventricle (LV) remodeling contributes to changes in systemic hemodynamics and may be influenced by altered regulatory role of renin-angiotensin system (RAS) and autonomic nervous system (ANS) in PreHT but otherwise healthy individuals. To distinguish high normal blood pressure effect from those considered normal or high, study will be performed in three groups of individuals: prehypertensive (BP 130-139/85-89 mmHg), hypertensive (stage I, BP 140-150/90-100 mmHg), and controls (BP less than or equal to 129/85 mmHg). Altogether, the impairment of normal vascular relaxation mechanisms, endothelial activation as well as vascular and LV remodeling could play crucial role in increased cardiovascular risk and CVDs incidence in PreHT individuals. Moreover, the prognostic significance of assessing endotehlial dysfunction in hypertension (as well as in PreHT) is yet to be established.

Oxidative stress and endoplasmic reticulum (ER) stress play a key role in tubular damage in both acute kidney injury and chronic kidney disease (CKD). Oxidative stress in the kidneys promotes renal vascular remodeling and increases preglomerular resistance. These are key elements in hypertension, acute and chronic kidney injury, as well as diabetic nephropathy. Chronic renal hypoxia is highlighted as the final common pathway to end-stage renal disease (ESRD). MicroRNA molecules (miRNA) also play an important role in these processes. MicroRNAs (miRNAs) are regulators of gene expression and play a role in the progression of renal ischemia-reperfusion injury. Although the pathophysiological contribution of microRNAs (miRNAs) to kidney damage has also been highlighted, the effect of miRNAs on kidney damage under conditions of oxidative and ER stress remains understudied.