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Kidney Inflammation, Injury and Regeneration
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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.
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Keywords
- 2-kidney-1-clip
- 2k1c
- acute and chronic kidney disease
- acute kidney failure
- acute kidney injury
- AKI
- allograft rejection
- alport syndrome
- Apoptosis
- arachidonic acid
- B-cell attracting chemokine
- biomarkers
- C-reactive protein
- cAMP Regulatory Element Binding Protein (CREB)
- chemerin
- Chronic Kidney Disease
- chronic kidney disease (CKD)
- chronic kidney injury
- Class IIa Histone Deacetylases (HDAC)
- CmklR1
- conditioned medium
- cPLA2 and COX-2
- CREB Regulated Transcriptional Coactivators (CRTC)
- CXCL13
- cyclooxygenase
- Cytochrome P450
- Cytotoxicity
- dapagliflozin
- Diabetes Mellitus
- diabetic kidney disease
- diabetic kidney diseases
- diabetic nephropathy
- Diagnostics
- differentiation
- DSS-colitis
- empagliflozin
- endotoxemia
- endotoxemia-induced oliguric kidney injury
- Epithelial Cells
- exosome
- Exosomes
- extracellular vesicles
- Farnesiferol B
- Fibrosis
- focal segmental glomerulosclerosis
- G-protein-coupled bile acid receptor (TGR5)
- genotype
- glomerular basement membrane
- glomerular damage
- glomerular filtration barrier (GFB)
- glomerular injury
- glomerulus
- GLP-1 receptor agonists
- haem
- hematuria
- Hypertension
- IgA nephropathy
- IL-18
- Inflammation
- Inflammatory Bowel Disease (IBD)
- inflammatory maker
- injury
- interleukin-6
- ischemia-reperfusion
- ischemia/reperfusion injury
- Kidney
- kidney inflammation
- kidney injury
- kidney proximal tubule
- kidney transplantation
- KIT assay
- KIT-IgA score
- lipoxygenase
- lncRNA
- long non-coding RNA
- long non-coding RNAs
- LPS-binding protein
- lysophosphatidic acid
- lysophosphatidic acid receptor
- mesenchymal stem cell
- mesenchymal stem cells
- Mesenchymal Stromal Cells
- mesodermal stem cell
- microRNA
- MicroRNAs
- miRNA
- modified-MSCs
- modifier gene
- molecular mechanisms
- molecular signaling
- myofibroblast
- n/a
- Natural Products
- necrosis
- nephrin
- niches
- NLRP3 inflammasome
- non-coding RNAs
- noninvasive
- Nuclear Factor kappa-light-chain-enhancer of activated B cells (NF-?B)
- obese kidney fibrosis
- omega-3 fatty acid
- Oxidative Stress
- papilla
- pericyte
- pigment nephropathy
- podocin
- podocyte
- polymorphism
- polyploidization
- polyunsaturated fatty acids
- prediction
- proximal tubule
- regulated necrosis
- renal cell carcinoma
- renal fibrosis
- renal inflammation
- renal injury
- renal ischemia-reperfusion
- renal progenitors
- renal stem cells
- renal tubular cells
- renovascular hypertension
- rhabdomyolysis
- ROS
- Salt Inducible Kinase (SIK)
- scattered tubular cells
- SGLT2 inhibitors
- signal transduction
- signaling cascade
- slit diaphragm
- stem cell
- T cell-mediated rejection
- Taiwan
- Therapeutic target
- therapeutics targets
- Thy1.1 nephritis
- transcription
- tubular injury
- type I collagen
- type IV collagen
- type V collagen
- xanthine oxidase
Links
DOI: 10.3390/books978-3-03928-539-6Editions
