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Despite being described for the first time more than 110 years ago, Chagas disease (caused by the parasite Trypanosoma cruzi) persists as one of the most neglected tropical diseases. This persistent neglect of those affected by this disease is evidenced by the ongoing scientific evidence gaps, the difficulty of incorporating new diagnostic and treatment technologies into the market, and public health failures to ensure timely access to diagnosis and treatment associated with the development of consistent surveillance and control actions. As a result, there is a high burden of morbidity and mortality, and poor quality of life, poverty, stigma, and a fear of death persist for affected people, both in endemic areas in Latin America, and in non-endemic areas. This book spans a variety of disciplines and contributes significantly to reducing the gap in scientific knowledge on Chagas disease, towards achieving the Sustainable Development Goals by 2030.

Medicine --- Chagas disease --- neglected tropical diseases --- migration --- healthcare rights --- mucosal leishmaniasis --- co-infection --- antimoniate therapy --- cardiomyopathy --- myocardial fibrosis --- myocardial sympathetic denervation --- inflammation --- sudden death --- cardiac magnetic resonance --- radionuclide imaging --- SPECT-CT --- PET-CT --- heart disease --- electrocardiogram --- disease progression --- stroke --- risk assessment --- Trypanosoma cruzi --- Triatoma infestans --- parasite prevalence --- coprophagy --- human illness --- neglected tropical disease --- global financing --- annual funding --- investments --- disease notification --- public policy --- neglected topical diseases --- healthcare access --- chagasic cardiomyopathy --- heart transplantation --- Chagas disease reactivation --- cardiac allograft rejection --- treatment of reactivation --- genome --- parasite --- neglected diseases --- heart transplant --- chagas disease reactivation --- Cohort studies --- Neglected diseases --- Dynamic programming --- cost of illness --- premature --- efficiency --- organizational --- life expectancy --- American trypanosomiasis --- Trypanosoma cruzi infection --- public health --- epidemiology --- prevention and control --- surveillance --- clinical research --- One Health --- Chagas disease --- neglected tropical diseases --- migration --- healthcare rights --- mucosal leishmaniasis --- co-infection --- antimoniate therapy --- cardiomyopathy --- myocardial fibrosis --- myocardial sympathetic denervation --- inflammation --- sudden death --- cardiac magnetic resonance --- radionuclide imaging --- SPECT-CT --- PET-CT --- heart disease --- electrocardiogram --- disease progression --- stroke --- risk assessment --- Trypanosoma cruzi --- Triatoma infestans --- parasite prevalence --- coprophagy --- human illness --- neglected tropical disease --- global financing --- annual funding --- investments --- disease notification --- public policy --- neglected topical diseases --- healthcare access --- chagasic cardiomyopathy --- heart transplantation --- Chagas disease reactivation --- cardiac allograft rejection --- treatment of reactivation --- genome --- parasite --- neglected diseases --- heart transplant --- chagas disease reactivation --- Cohort studies --- Neglected diseases --- Dynamic programming --- cost of illness --- premature --- efficiency --- organizational --- life expectancy --- American trypanosomiasis --- Trypanosoma cruzi infection --- public health --- epidemiology --- prevention and control --- surveillance --- clinical research --- One Health

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Acute kidney injury (AKI) is still associated with high morbidity and mortality incidence rates, and also bears an elevated risk of subsequent chronic kidney disease. Although the kidney has a remarkable capacity for regeneration after injury and may recover completely depending on the type of renal lesions, the options for clinical intervention are restricted to fluid management and extracorporeal kidney support. The development of novel therapies to prevent AKI, to improve renal regeneration capacity after AKI, and to preserve renal function is urgently needed. The Special Issue covers research articles that investigated the molecular mechanisms of inflammation and injury during different renal pathologies, renal regeneration, diagnostics using new biomarkers, and the effects of different stimuli like medication or bacterial components on isolated renal cells or in vivo models. The Special Issue contains important reviews that consider the current knowledge of cell death and regeneration, inflammation, and the molecular mechanisms of kidney diseases. In addition, the potential of cell-based therapy approaches that use mesenchymal stromal/stem cells or their derivates is summarized. This edition is complemented by reviews that deal with the current data situation on other specific topics like diabetes and diabetic nephropathy or new therapeutic targets.

microRNAs --- n/a --- transcription --- ischemia/reperfusion injury --- DSS-colitis --- kidney inflammation --- therapeutics targets --- CXCL13 --- glomerulus --- interleukin-6 --- rhabdomyolysis --- IgA nephropathy --- CREB Regulated Transcriptional Coactivators (CRTC) --- slit diaphragm --- injury --- xanthine oxidase --- Salt Inducible Kinase (SIK) --- acute and chronic kidney disease --- therapeutic target --- KIT-IgA score --- G-protein-coupled bile acid receptor (TGR5) --- lysophosphatidic acid --- glomerular injury --- IL-18 --- mesenchymal stem cells --- Taiwan --- acute kidney injury --- renal ischemia-reperfusion --- long non-coding RNA --- fibrosis --- acute kidney failure --- diabetic kidney diseases --- chronic kidney disease --- lncRNA --- LPS-binding protein --- endotoxemia-induced oliguric kidney injury --- dapagliflozin --- cPLA2 and COX-2 --- NLRP3 inflammasome --- CmklR1 --- haem --- chronic kidney injury --- omega-3 fatty acid --- noninvasive --- inflammation --- regulated necrosis --- GLP-1 receptor agonists --- miRNA --- AKI --- SGLT2 inhibitors --- diabetic kidney disease --- extracellular vesicles --- podocin --- type IV collagen --- epithelial cells --- nephrin --- 2-kidney-1-clip --- renal fibrosis --- papilla --- diagnostics --- necrosis --- non-coding RNAs --- podocyte --- Thy1.1 nephritis --- KIT assay --- oxidative stress --- conditioned medium --- C-reactive protein --- pericyte --- myofibroblast --- Nuclear Factor kappa-light-chain-enhancer of activated B cells (NF-?B) --- endotoxemia --- modifier gene --- polymorphism --- renal stem cells --- kidney --- polyploidization --- Class IIa Histone Deacetylases (HDAC) --- 2k1c --- molecular signaling --- proximal tubule --- arachidonic acid --- empagliflozin --- tubular injury --- signaling cascade --- signal transduction --- inflammatory maker --- niches --- biomarkers --- renal progenitors --- type V collagen --- cyclooxygenase --- focal segmental glomerulosclerosis --- inflammatory bowel disease (IBD) --- chronic kidney disease (CKD) --- allograft rejection --- renovascular hypertension --- genotype --- molecular mechanisms --- ROS --- prediction --- glomerular filtration barrier (GFB) --- alport syndrome --- scattered tubular cells --- long non-coding RNAs --- renal inflammation --- lysophosphatidic acid receptor --- cAMP Regulatory Element Binding Protein (CREB) --- Farnesiferol B --- differentiation --- mesenchymal stromal cells --- modified-MSCs --- kidney transplantation --- polyunsaturated fatty acids --- apoptosis --- type I collagen --- diabetes mellitus --- natural products --- lipoxygenase --- stem cell --- T cell-mediated rejection --- exosomes --- renal injury --- obese kidney fibrosis --- kidney injury --- cytotoxicity --- mesenchymal stem cell --- pigment nephropathy --- mesodermal stem cell --- ischemia-reperfusion --- cytochrome P450 --- renal cell carcinoma --- hematuria --- B-cell attracting chemokine --- microRNA --- chemerin --- glomerular basement membrane --- glomerular damage --- renal tubular cells --- kidney proximal tubule --- exosome --- hypertension --- diabetic nephropathy