Inhalt: | Prevalence and burden of chronic kidney disease -- Pathomorphism and evaluation of renal fibrosis -- Endothelial cells and renal fibrosis -- Mesangial cells and renal fibrosis -- Podocyte injury and glomerular sclerosis -- Tubular epithelial cell injury and renal fibrosis -- Monocyte-macrophages and renal fibrosis -- Pericytes and renal fibrosis -- Myofibroblast: Origin and regulation in renal fibrosis -- Mitochondrial lesion and renal fibrosis -- Metabolic nuclear receptors and renal fibrosis -- Role of renin angiotensin system in renal fibrosis -- Role of aldosterone in renal fibrosis -- TGF-β1 and renal fibrosis -- Connective tissue growth factor and renal fibrosis -- Lipid metabolism disorder and renal fibrosis -- Renal interstitial lymphangiogenesis in renal fibrosis -- Cell apoptosis and autophagy in renal fibrosis -- Pyroptosis and renal fibrosis -- Cell cycle arrest and renal fibrosis -- Inflammatory mediators and renal fibrosis -- Role of inflammasome in chronic kidney disease -- Oxidative stress and renal fibrosis -- Hypoxia and renal tubulointerstitial fibrosis -- Proteinuria and progression of chronic kidney disease -- Hypertension and renal fibrosis -- Diabetic Kidney disease and renal fibrosis -- Chronic allograft nephropathy and renal fibrosis -- Polycystic kidney disease and renal fibrosis -- Acute kidney injury and renal fibrosis -- Senescence and renal fibrosis -- Urinary biomarkers of renal fibrosis -- New therapies for the treatment of renal fibrosis This book systemically presents the latest research on renal fibrosis, covering all the major topics in the field, including the possible mechanisms, biomarkers, and strategies for prevention and treatment of chronic kidney disease (CKD). Due to its high prevalence, CKD represents a huge global economic and social burden. Irrespective of the initial causes, CKD progresses to end stage kidney disease (ESKD) due to renal fibrosis, which is characterized by glomerulosclerosis, tubule atrophy and atresia, and the excessive accumulation of extracellular matrix (ECM) in the kidney. Unfortunately, an estimated 1%-2% of the adult population living with CKD will need renal replacement therapy at some point as a result of ESKD. As such, strategies for preventing or slowing CKD progression to ESKD are of utmost importance, and studies aiming to understand the mechanisms of renal fibrosis have been the focus of intensive research. Recently, novel insights into the pathophysiological processes have furthered our understanding of the pathogenesis of renal fibrosis, and more importantly, promoted studies on the early diagnosis and treatment of CKD. This book draws lessons from the extensive, state-of-the-art research in this field, elaborating the new theories and new techniques to offer readers a detailed and comprehensive understanding of renal fibrosis and as well as inspiration for future research directions |
