4 edition of Cellular Stress Responses In Renal Diseases (Contributions to Nephrology) found in the catalog.
June 17, 2005
by S. Karger AG (Switzerland)
Written in English
|Contributions||Mohammed S. Razzaque (Editor), Takashi Taguchi (Editor)|
|The Physical Object|
|Number of Pages||158|
Response Of Renal Cells To Osmotic Stress Burg, Maurice Benjam National Heart, Lung, and Blood Institute. Search 23 grants from Maurice Burg Search grants from National Heart, Lung, and Blood Institute Therapeutic Interventions to Access Outcomes and Disparities in Chronic Kidney Disease Among Veterans. End-stage renal disease (ESRD) is associated with significantly increased morbidity and mortality resulting from cardiovascular disease (CVD) and infections, accounting for 50% and 20%, respectively, of the total mortality in ESRD patients. It is possible that these two complications are linked to alterations in the immune system in ESRD, as uremia is associated with a state of immune.
Basic science data suggest that acute kidney injury (AKI) induced by ischemia-reperfusion injury (IRI) is an inflammatory process involving the adaptive immune response. Little is known about the T-cell contribution in the very early phase, so we investigated if tubular cellular stress expressed by elevated cell cycle biomarkers is associated with early changes in circulating T-cell . Chronic kidney disease (CKD) is characterized by an irreversible decrease in kidney function and induction of various metabolic dysfunctions. Accumulated findings reveal that chronic hypoxic stress and endoplasmic reticulum (ER) stress are involved in a range of pathogenic conditions, including the progression of CKD. Because of the presence of an arteriovenous oxygen shunt, the kidney is.
Renal disease in cocaine and heroin users is associated with the nephrotic syndrome, acute glomerulonephritis, amyloidosis, interstitial nephritis, and rhabdomyolysis. The pathophysiologic basis of cocaine-related renal injury involves renal hemodynamic changes, glomerular matrix synthesis and degradation, and oxidative stress and induction of renal atherogenesis. Heroin is the most commonly. Plasma cell dyscrasias represent a group of diseases characterized by the clonal expansion of abnormal plasma cells. The result of this clonal expansion is the overproduction of a monoclonal (M) protein which could be either the whole immunoglobulin or a fragment (heavy or light chain alone). Thus, these disorders are also collectively referred to as monoclonal gammopathies.
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Cellular stress responses in renal diseases. Basel ; New York: Karger, © Cellular Stress Responses In Renal Diseases book Online version: Cellular stress responses in renal diseases.
Basel ; New York: Karger, © (OCoLC) Material Type: Internet resource: Document Type: Book, Internet Resource: All Authors / Contributors: Mohammed S Razzaque; Takashi Taguchi. Get this from a library.
Cellular stress responses in renal diseases. [Mohammed S Razzaque; Takashi Taguchi;] -- Heat shock proteins are a distinctive class of proteins that have evolved to cope with stress and to provide cellular defense against a wide range of cell injuries.
Cellular stress responses. Stress and chronic diseases. Excessive amounts of ROS, overloading of the peroxidized polyunsaturated fatty acids (hydroxynonenals), products of cholesterol oxidation, mutations favoring protein misfolding, altered glycosylation, etc. may cause a severe stress and lead to accumulation of unfolded or misfolded proteins in brain cells .The so called ‘aggregated proteins’ accumulation is a Cited by: The aim of this study was to determine whether PrP C could serve as a urinary ER stress biomarker for ER stress-mediated kidney diseases by studying a combination of cellular Cited by: 1.
Aging is the main risk factor for cardiovascular diseases (CVD), and senescence in endothelial cells seems to be an initial step in the cascade of events that will culminate with the development of these pathologies.
In this chapter, we examine the pathophysiological mechanism(s) involved in endothelial senescence, leading to CVD as well as the biochemical and cellular pathways Cited by: 3. Survived renal tubular cells that are sublethally injured activate the so-called renal stress response, an intrinsic cytoprotective response that increases the cell's chance of survival, transforming potentially lethal cellular insults into sublethal forms of cell injury.
The renal stress response, in addition to other adaptive mechanisms of. Insufficient cellular stress adaptation may underpin the persistent activation of inflammatory and fibrogenic signaling in damaged kidneys. We propose that harnessing cellular stress-adaptive responses will be a promising therapeutic strategy to halt or.
Stress can be physiological (infection, injury, disease), or psychological (anxiety, argument, conflict, threats to personal safety or well-being). Living with a chronic illness, such as kidney disease, or learning for the first time that you have a chronic illness can be a significant source of stress.
stress responses, especially in mitochondria, endoplasmic reticul a (ER), and primary cilia, are deeply involved in kidney disease pathophysiology. Mitochondria are the center of energy production in most eukaryotic cells.
Renal proximal tubular cells are highly energy-demanding and abundant in mitochondria. Mitochondrial dysfunctions in. SUMMARY: Insufficient cellular stress adaptation may underpin the persistent activation of inflammatory and fibrogenic signaling in damaged kidneys.
We propose that harnessing cellular stress-adaptive responses will be a promising therapeutic strategy to halt or even reverse the deleterious process of AKI-to-CKD transition.
These cells might contribute to inflammation and destabilization of atherosclerotic plaques, and have, therefore, been identified as novel nonclassical cardiovascular risk factors. The cellular composition of the immune system does not normalize after successful kidney transplantation despite a rapid reduction in inflammation and oxidative stress.
Although p53 is regulated by an array of post-translational modifications, both during normal homeostasis and in stress-induced responses 2,3,4, how p53 maintains its. Diseases of any component of the brain (including the cerebral hemispheres, diencephalon, brain stem, and cerebellum) or the spinal cord.
| Explore the latest full-text research PDFs, articles. Serine/threonine-protein kinase Sgk1 also known as serum and glucocorticoid-regulated kinase 1 is an enzyme that in humans is encoded by the SGK1 gene. SGK1 belongs to a subfamily of serine/threonine kinases that is under acute transcriptional control by several stimuli, including serum and kinase is activated by insulin and growth factors via phosphatidylinositide Abstract.
The zebrafish is a useful genetic and embryological model system for investigating renal development, regeneration, and disease. In Zebrafish, kidney development progresses through two types of kidney: the pronephros, a fully functional, two-nephron embryonic kidney and the mesonephros, the adult kidney comprising hundreds of nephrons.
Oxidative stress is associated with many renal disorders, both acute and chronic, and has also been described to contribute to the disease progression. Therefore, oxidative stress is a potential therapeutic target. The human antioxidant α1-microglobulin (A1M) is a plasma and tissue protein with heme-binding, radical-scavenging and reductase activities.
A1M can be internalized by cells. Erythropoietin (/ ɪ ˌ r ɪ θ r oʊ ˈ p ɔɪ. ɪ t ɪ n,-r ə-,-p ɔɪ ˈ ɛ t ɪ n,-ˈ iː t ɪ n /; EPO), also known as erythropoetin, haematopoietin, or haemopoietin, is a glycoprotein cytokine secreted mainly by the kidney in response to cellular hypoxia; it stimulates red blood cell production (erythropoiesis) in the bone levels of EPO (around 10 mU/mL) are constantly.
Stress in the body’s cells is both the cause and consequence of inflammatory diseases or cancer. The cells react to stress to protect themselves. Researchers have now developed a new technique. ROS and oxidative stress play a vital role in the pathogenesis of acute kidney injury and chronic kidney disease, and it is well documented that increased oxidative stress in patients enhances the progression of renal diseases.
Oxidative stress activates autophagy, which facilitates cellular adaptation and diminishes oxidative damage by. For more than a decade, Naviaux and colleagues have been investigating and developing a theory based on cell danger response (CDR), a natural and universal cellular reaction to injury or stress.
In the new paper, Naviaux describes the metabolic features of the three stages of CDR that comprise the healing cycle. Cellular adaptation is the ability of cells to respond to various types of stimuli and adverse environmental changes.
These adaptations include hypertrophy (enlargement of individual cells), hyperplasia (increase in cell number), atrophy (reduction in size and cell number), metaplasia (transformation from one type of epithelium to another), and dysplasia (disordered growth of cells).Title: Therapeutical Relevance of MAP-Kinase Inhibitors in Renal Diseases: Current Knowledge and Future Clinical Perspectives VOLUME: 15 ISSUE: 20 Author(s):M.
Teresa Grande and Jose M. Lopez-Novoa Affiliation:Departamento de Fisiologia y Farmacologia, Universidad de Salamanca, Avda, Campo Charro s/n, Salamanca, Spain. Keywords:Acute renal failure, chronics renal failure. A renal disease can be attributed to a variety of causes which, include genetics, injuries and medicine.
Find a full list of kidney problems.