[Signaling pathways in renal fibrosis]
ROKONAY Réka, SZIKSZ Erna, LIPPAI Rita, PAP Domonkos, VERES-SZÉKELY Apor, REUSZ György, SZABÓ Attila, VANNAY Ádám
SEPTEMBER 20, 2014
Hypertension and nephrology - 2014;18(03-04)
ROKONAY Réka, SZIKSZ Erna, LIPPAI Rita, PAP Domonkos, VERES-SZÉKELY Apor, REUSZ György, SZABÓ Attila, VANNAY Ádám
SEPTEMBER 20, 2014
Hypertension and nephrology - 2014;18(03-04)
[Myofibroblasts are the main effector cells of tissue fibrosis in chronic kidney disease. These cells are the main source of collagen rich extracellular matrix in the fibrous tissue. Recent hypotheses suggest that pericytes are the major progenitors of myofibroblasts. Platelet derived growth factor, transforming growth factor β and Wingless/Int signaling pathways play important role in pericyte activation. There are experimental evidences that blocking this pathways inhibits tissue fibrosis, therefore they might be targets for the development of antifibrotic drugs in the future.]
Hypertension and nephrology
[Recently we have in vivo visualized glomerular filtration and fluid flow from the JGA portion of afferent arteriole into JGA using intravital multiphoton microscopy. Fluorescence of the extracellular fluid marker lucifer yellow appeared in the interstitium around the distal portion of afferent arteriole before the filtration into Bowman's capsule. In isolated microperfused JGA we demonstrated fluid movement from the glomerulus into the MD tubule. All these prove that there is a significant and dynamic fluid flow exists in the JGA. Angiotensin II similar to VEGF plays a role in regulation of permeability/fenestration formation. Angiotensin II acts through AT1 receptor and PV-1 protein synthesis.]
Hypertension and nephrology
[Hantaviruses are widespread infectious agents carried by different rodent species. The majority of them belongs to viral zoonotic pathogens, sometimes causing severe human infections. Hantaviruses inflict hemorrhagic fever with renal syndrome in Eurasia and supposedly in Africa, and hantavirus cardio-pulmonary syndrome in the Americas. The relationship between the virus and its host species is a result of a several million year co-evolution. Although virus replication is most intense in the infected rodents' lungs, these animals do not develop disease, instead they carry and spread the pathogens throughout their lifetime by body fluids. In the majority of infections, the virus gets into the human body by vaporization of rodent body fluids or by direct contact. In Europe, Puumala (PUUV) and Dobrava-Belgrade (DOBV) hantaviruses are the most abundant hantaviral infectious agents. There are numerous studies described the presence of different genotipes of hantaviruses circulating in Hungary. Although the number of clinical and epidemiolgical studies are limited, the medical importance - especially in a high risk population - of these viruses are unqustionable. There are a variety of methods to identify hantaviral infections. Molecular biological methods (RT-PCR) - also enabling genotyping - and virus neutralization tests proved to be the most reliable tools. The latter technique requires virus culturing, which can only be carried out in high-containment laboratories.]
Hypertension and nephrology
[The author summarizes knowledge about Reynolds risk assessment system based on data of references and own experiences. The first part of article is about how the results of study of pathogenesis of atherosclerosis were converted into new risk assessment systems. One result of this process is the Reynolds system wich is consisted of traditional riks factors, high sensitive C-reactive protein and the patients’ family medical history. He demonstrates essence of Reynolds system and process of it’s validity. The author deals with comparison of Reynolds system with other traditional risk assessment systems. The practical issues of application of Reynolds system are detailed in the conclusion of the article.]
Hypertension and nephrology
Hypertension and nephrology
[Objectives: To evaluate a possible link between serum uric acid (SUA) levels, arterial stiffness and atherogenic index of plasma on one hand and renal function on the other and to test the role of SUA in the assessment of total cardiovascular risk. Materials and methods: We studied serum uric acid levels (SUA) in 1975 subjects included in SEPHAR II survey. We measured arterial stiffness parameters, calculated atherogenic index of plasma and estimated glomerular filtration rate (eGFR) by MDRD and CKD-EPI formulae and assessed total cardiovascular risk according to current ESH-ESC risk stratification chart. Results: The highest SUA values were recorded in subjects with grade III HT and were correlated with increased arterial stiffness and with increased atherogenic index of plasma. The lowest eGRF values, assessed by both MDRD and CKD-EPI, were observed among subjects with hyperuricemia and a significant indirect correlation between SUA and eGFR was evidenced. A proportional correlation between SUA values and total CV risk was also obtained. Conclusions: The study supports SUA implication in the pathogenesis of elevated blood pressure and the role of uric acid as a cardiovascular risk factor, particularly for the development of hypertension and renal disease.]
Clinical Neuroscience
[The souvenirs of Hans Selye as a teacher of graduate and post graduate students are presented and discussed. The main aim of his teaching was to orient the student toward importance and originality of findings.]
Hypertension and nephrology
[The high incidence of chronic kidney diseases and, regardless of the etiology, their progression to renal fibrosis with end-stage renal failure rise the urgent need to reveal the pathomechanisms. As the disease leads to complex changes in the body, it is essential to use in vivo model systems for these investigations. Animal experiments choosing the appropriate model system helps to develop more sensitive early diagnostic markers and new therapeutic approaches. Several animal experimental model descriptions can be found in the literature, which mimic specific or more general human diseases in order to help the better understanding of the pathomechanisms. Using these model systems, we are able to analyze the detailed pathophysiology of glomerulonephritis, tubulointerstitial fibrosis, glomerular scarring or generalized renal fibrosis. The most commonly used model systems for renal fibrosis are presented and discussed.]
Hypertension and nephrology
[Epithelial-mesenchymal transition (EMT) plays a central role in physiological and pathological processes of embryogenesis, carcinogenesis and tissue fibrosis. During EMT epithelial cells may transform to myofibroblasts, which are the effector cells of fibrosis. In our summary the process of EMT and its medical importance will be reviewed in relation to renal fibrosis. Regardless of the initiating cause the final common mechanism of organ fibrosis is similar in the different chronic renal diseases. It always involves major inflammatory responses, however the molecular mechanisms involved are still elusive. The EMT now takes centre stage as the point of convergence between inflammation and the progression of degenerative fibrotic diseases. Understanding the pathomechanism of EMT and the significance of signalling pathways involved in this process may lead to a new therapeutic approach in the treatment of chronic renal diseases.]
Hypertension and nephrology
[There are about a quarter of million patients who need chronic renal replacement therapy in Europe, and the estimated number of patients with chronic kidney disease is about tenfold higher. Interestingly, regardless of the initiating cause the mechanism of fibrosis is similar to each other in the different chronic kidney diseases. In general, the damaged glomerular or tubular cells release danger signals and produce chemotactic stimuli, which trigger the rapid recruitment of leukocytes. The infiltrating immune cells and the damaged renal cells then produce high levels of proinflammatory cytokines, growth factors, chemokines and adhesion molecules which contribute to glomerular/tubular injury, accumulation of further leukocytes and myofibroblasts, which are the effector cells of renal fibrosis. However the origin of myofibroblasts is still controversial. Recent hypotheses suggest that they are originated from different renal cells, such as epithelial and endothelial cells, pericytes or bone marrow derived fibrocytes. The myofibroblasts thus generated serve as key cellular mediators of renal fibrosis. Myofibroblasts have migratory capacity, are resistant to apoptosis, produce several growth factors and cytokines and according to our present knowledge these cells are the main source of collagen-I and -III rich extracellular matrix in the fibrous tissue. Organ fibrosis is characterized with excessive deposition of extracellular matrix leading to glomerular sclerosis and renal tubulointerstitial fibrosis. The excessive deposition of fibrous tissue replaces healthy kidney tissue; nephrons disappear and kidney function declines gradually. In this article the knowledge is summarized on the molecular changes leading to the generation of renal myofibroblasts.]
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