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Adipose tissue is a rich, ubiquitous, and easily accessible source for multipotent mesenchymal stromal/stem cells (MSCs), so-called adipose-derived stromal/stem cells (ASCs). Primary isolated ASCs are a heterogeneous preparation consisting of several subpopulations of stromal/stem and precursor cells. Donor-specific differences in ASC isolations and the lack of culture standardization hinder the comparison of results from different studies. Nevertheless, ASCs are already being used in different in vivo models and clinical trials to investigate their ability to improve tissue and organ regeneration. Many questions concerning their counterparts and biology in situ, their differentiation potential in vitro and in vivo, and the mechanisms of regeneration (paracrine effects, including regeneration-promoting factors and extracellular vesicles, differentiation, and immunomodulation) are not completely understood or remain unanswered. This Special Issue covers research articles investigating various adipose tissues as a source for ASC isolation, specific cultures methods to enhance proliferation or viability, and the differentiation capacity. Furthermore, other studies highlight aspects of various diseases, the immunosuppressive potential of ASCs and their derivates, or the in vivo tracking of transplanted ASCs. This edition is complemented by a review that summarizes the current knowledge of spheroid culture system methods and applications for mesenchymal stem cells.

Medicine --- lipomas --- adipose tissue --- stem cells --- adipogenesis --- osteogenesis --- mesenchymal stem cells --- T-cells --- conditioned medium --- extracellular vesicles --- TLR --- INF-γ --- adipose-derived stromal cells --- equine metabolic syndrome --- metformin --- adipose-derived stem cells --- adipocytes --- differentiation --- collagen I --- adiponectin --- integrins --- discoidin domain-containing receptor --- ageing --- subcutaneous fat --- adipose tissue-derived mesenchymal stromal/stem cells (ASCs) --- cell differentiation --- volatile organic compounds --- metabolic monitoring --- adipose-derived stromal/stem cells --- chondrogenesis --- colony forming unit-fibroblast --- fetal bovine serum --- human platelet lysate --- mesenchymal stem cell --- regenerative medicine --- human adipose-derived stem cells --- stem cell proliferation --- signaling pathway --- adipose-derived mesenchymal stem cells --- migration --- secretion --- primary cilium --- sonic hedgehog signaling --- mesenchymal stromal/stem cells --- perirenal --- fat --- characterization --- stimulation --- lipopolysaccharide --- cytokines --- cytomegalovirus --- angiogenesis --- adipose derived mesenchymal cells --- Histogel --- 3D cell culture --- spheroid culture --- biomaterials --- phenotype --- secretory potential --- ankylosing spondylitis --- systemic lupus erythematosus --- systemic sclerosis --- mesenchymal stromal cells --- breast cancer --- tumor microenvironment --- perineural invasion --- adipose derived stem cells --- valproic acid --- protein interactions --- MAPK pathway --- JAK/STAT pathway --- mesenchymal stromal cell --- tissue of origin --- prolonged culture --- epigenetic memory --- tracking --- bio imaging --- bioluminescence --- qRT-PCR --- Ataxia telangiectasia --- Atm --- n/a

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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

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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 chronic kidney disease in the sequel. Whereas 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—in both the short- and long-term—is urgently needed. This Special Issue includes papers investigating the pathological mechanisms of renal inflammation and AKI and diagnostics using new biomarkers. Furthermore, experimental in vitro and in vivo studies examining potential new approaches to attenuate kidney dysfunction are included, as well as review articles.

inflammation --- chronic kidney disease --- anemia --- anemia of inflammation --- ESA hyporesponsiveness --- renal tubular epithelial cells --- macrophages --- lipocalin-2 --- iron --- cilastatin --- hypoxia inducible factor-1-α --- ischemia-reperfusion injury --- acute kidney injury --- cyclophilin A --- fibrosis --- renal fibrosis --- tubular necrosis --- preeclampsia --- podocytes --- VEGF --- FSGS --- proteinuria --- endocan --- ESM-1 --- renal replacement therapy --- kidney transplantation --- biomarker --- diabetic nephropathy --- focal segmental glomerulosclerosis --- innate immunity --- membranous nephropathy --- minimal change diseases --- TLR --- NOX1 --- ML171 --- reactive oxygen species --- ERK --- T cells --- glomerulonephritis --- chemokines --- renal disease --- DJ-1 --- ND-13 --- renal inflammation --- oxidative stress --- UUO --- autophagy --- apoptosis --- trehalose --- simvastatin --- endotoxin --- tubular apoptosis --- cytochrome C --- Bcl-XL --- survivin --- hypercholesterolemia --- xanthine oxidase --- NF-κB pathway --- tertiary lymphoid organs --- B cells --- BAFF --- kidney fibrosis --- myofibroblast activation --- extracellular matrix --- Hippo pathway --- verteporfin --- IgAN --- CKD --- progression --- ACEI --- corticosteroids --- costimulation --- coinhibition --- kidney transplant --- SPR --- protein binding affinity --- adaptive immunity --- epithelial-to-mesenchymal transition --- E. cava extracts --- dieckol --- spontaneously hypertensive rats --- angiotensin II --- n/a