Vivette Denise D’Agati
Department of Pathology and Cell Biology, Columbia University, New York, New York, USA. | Department of Pathology and Cell Biology, Columbia University Irving Medical Center, ...
KOL Resume for Vivette Denise D’Agati
Department of Pathology and Cell Biology, Columbia University, New York, New York, USA.
Department of Pathology, Columbia University Irving Medical Center, New York, NY 10032, USA.
Pathology and Cell Biology, Columbia University Irving Medical Center, New York, NY, USA
Department of Pathology, College of Physicians and Surgeons, Columbia University, New York, NY, USA
Columbia University School of Medicine, New York City, New York.
Department of Pathology, Columbia University Medical Center, New York, NY
Renal Pathology Laboratory, Columbia University Medical Center, New York, New York, USA.
Columbia University School of Medicine, New York City, New York
Department of Pathology Cell Biology, Columbia University Medical Center, New York, New York, USA
Department of Pathology, Renal Pathology Laboratory, Columbia University College of Physicians and Surgeons, New York, NY
From Columbia University, New York, New York; VU University Medical Center, Amsterdam, the Netherlands; Nephrology Associates, Newark, Delaware; Krysiewicza Children's Hospital, Poznań, Poland; Poznań University of Medical Sciences and Center for Medical Genetics GENESIS, Poznań, Poland; IRCCS Giannina Gaslini Children's Hospital, Genova, Italy; IRCCS San Raffaele Scientific Institute, Milan, Italy; New York University School of Medicine, New York, New York; University of Texas Southwestern Medical Center, Dallas, Texas; and French Institute of Health and Medical Research (INSERM) U1163, Paris Descartes-Sorbonne Paris Cité University, Imagine Institute, and Necker Hospital, Paris, France.
Department of Pathology and Cell Biology, College of Physicians and Surgeons, Columbia University, New York, NY, 10032, USA
Renal Pathology Laboratory, College of Physicians and Surgeons, Columbia University, New York, New York
Department of Pathology, Columbia University Medical Center, New York, New York;
Mayo Clinic, Rochester, Minnesota
Department of Pathology, College of Physicians and Surgeons of Columbia University, New York, New York
Vivette Denise D’Agati: Influence Statistics
|nephrin podocyte viability||#1|
|ischemic nlrp3 inflammasome||#1|
|severity interstitial inflammation||#1|
|antiretroviral naive adults||#1|
|hivan knockout mice||#1|
|klf15 cell differentiation||#1|
|yesassociated protein fsgs||#1|
|cdc retrospective analysis||#1|
|hepatic ischemia liver||#1|
|indolent monoclonal igg1κ||#1|
|murine diabetic kidney||#1|
|ckd stage nsg||#1|
|plasma norepinephrine mice||#1|
|monocytes mφs cns||#1|
|isoflurane renal ischemia||#1|
|gtl peripheral lesions||#1|
|pad4deficient mice renal||#1|
|early expression pkd2||#1|
|monoclonal igg deposits||#1|
|isoflurane multiorgan injury||#1|
|renal protection mice||#1|
|crystalline nephropathy treatment||#1|
|ret receptor misexpression||#1|
|2400 children adults||#1|
|persistent activity chronicity||#1|
|category agreement 64||#1|
|nphs2 susceptibility loci||#1|
|tissues organs development||#1|
|metabolic creatinine diagnosis||#1|
|50 reduction proteinuria||#1|
|urine acidification mice||#1|
|fh1 domain dia1||#1|
|glomerular injury injury||#1|
|tcr periglomerular regions||#1|
|renal wt mice||#1|
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Prominent publications by Vivette Denise D’Agati
Differential expression of cyclin-dependent kinase inhibitors in human glomerular disease: role in podocyte proliferation and maturation.
[ PUBLICATION ]
BACKGROUND: Normal human podocytes are terminally differentiated and quiescent cells. It is not known why podocytes fail to proliferate in response to most forms of injury. Proliferation is regulated by cell cycle proteins and their inhibitors. The Cip/Kip family of cyclin-dependent kinase (CDK) inhibitors (p21, p27, p57) in general prevent proliferation by inhibiting cyclin-CDK complexes. In the current study, we determined the expression and possible role of specific CDK inhibitors in ...
|Known for Podocyte Proliferation | Kinase Inhibitor | Glomerular Disease | P27 P57 | Differential Expression|
GDNF signaling through the Ret receptor tyrosine kinase (RTK) is required for ureteric bud (UB) branching morphogenesis during kidney development in mice and humans. Furthermore, many other mutant genes that cause renal agenesis exert their effects via the GDNF/RET pathway. Therefore, RET signaling is believed to play a central role in renal organogenesis. Here, we re-examine the extent to which the functions of Gdnf and Ret are unique, by seeking conditions in which a kidney can develop ...
|Known for Kidney Development | Gdnf Ret | Renal Agenesis | Etv4 Etv5 | Proteins Mice|
SGLT2 Protein Expression Is Increased in Human Diabetic Nephropathy SGLT2 PROTEIN INHIBITION DECREASES RENAL LIPID ACCUMULATION, INFLAMMATION, AND THE DEVELOPMENT OF NEPHROPATHY IN DIABETIC MICE*
[ PUBLICATION ]
There is very limited human renal sodium gradient-dependent glucose transporter protein (SGLT2) mRNA and protein expression data reported in the literature. The first aim of this study was to determine SGLT2 mRNA and protein levels in human and animal models of diabetic nephropathy. We have found that the expression of SGLT2 mRNA and protein is increased in renal biopsies from human subjects with diabetic nephropathy. This is in contrast to db-db mice that had no changes in renal SGLT2 ...
|Known for Diabetic Nephropathy | Sglt2 Inhibition | Renal Lipid | Protein Expression | Db Mice|
RAGE modulates myocardial injury consequent to LAD infarction via impact on JNK and STAT signaling in a murine model
[ PUBLICATION ]
The receptor for advanced glycation end-products (RAGE) has been implicated in the pathogenesis of ischemia-reperfusion (I/R) injury in the isolated perfused heart. To test the hypothesis that RAGE-dependent mechanisms modulated responses to I/R in a murine model of transient occlusion and reperfusion of the left anterior descending coronary artery (LAD), we subjected male homozygous RAGE(-/-) mice and their wild-type age-matched littermates to 30 min of occlusion of the LAD followed by ...
|Known for Myocardial Injury | Murine Model | Rage Mice | 48 Reperfusion | Advanced Glycation|
Acute and delayed renal protection against renal ischemia and reperfusion injury with A1 adenosine receptors
[ PUBLICATION ]
We showed previously that activation of A(1) adenosine receptors (AR) protects against renal ischemia-reperfusion (IR) injury in rats and mice. In the heart, transient A(1)AR activation produces biphasic protective effects: acute protection wanes after several hours but protective effects return 24-72 h later (second window of protection). In this study, we determined whether A(1)AR activation produces delayed renal protection and elucidated the mechanisms of acute and delayed renal ...
|Known for Renal Protection | Adenosine Receptors | A1ar Activation | Reperfusion Injury | Protective Effects|
BACKGROUND AND OBJECTIVES: Renal biopsies performed in diabetic patients are increasing in number and complexity. This study sought to determine the usefulness of renal biopsy in patients with diabetes and the predictability of diagnosing diabetic nephropathy (DN) versus nondiabetic renal disease (NDRD) from clinical and laboratory data.
DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: To assess modern trends, a retrospective study was performed of clinical-pathologic findings in all ...
|Known for Dn Ndrd | Renal Biopsy | Modern Spectrum | Hypertensive Nephrosclerosis | Iga Nephropathy|
Ischemic Preconditioning Provides Both Acute and Delayed Protection against Renal Ischemia and Reperfusion Injury in Mice
[ PUBLICATION ]
Acute as well as delayed ischemic preconditioning (IPC) provides protection against cardiac and neuronal ischemia reperfusion (IR) injury. This study determined whether delayed preconditioning occurs in the kidney and further elucidated the mechanisms of renal IPC in mice. Mice were subjected to IPC (four cycles of 5 min of ischemia and reperfusion) and then to 30 min of renal ischemia either 15 min (acute IPC) or 24 h (delayed IPC) later. Both acute and delayed renal IPC provided ...
|Known for Renal Ischemia | Reperfusion Injury | Ischemic Preconditioning | Delayed Ipc | Protection Acute|
Dominant effects of RET receptor misexpression and ligand-independent RET signaling on ureteric bud development.
[ PUBLICATION ]
During kidney development, factors from the metanephric mesenchyme induce the growth and repeated branching of the ureteric bud, which gives rise to the collecting duct system and also induces nephrogenesis. One signaling pathway known to be required for this process includes the receptor tyrosine kinase RET and co-receptor GFR(&agr)-1, which are expressed in the ureteric bud, and the secreted ligand GDNF produced in the mesenchyme. To examine the role of RET signaling in ureteric bud ...
|Known for Ureteric Bud | Ret Receptor | Knockout Mice | Kidney Development | Metanephric Mesenchyme|
GATA-1 is a zinc-finger transcription factor believed to play an important role in gene regulation during the development of erythroid cells, megakaryocytes and mast cells. Other members of the GATA family, which can bind to the same DNA sequence motif, are co-expressed in several of these hemopoietic lineages, raising the possibility of overlap in function. To examine the specific roles of GATA-1 in hematopoietic cell differentiation, we have tested the ability of embryonic stem cells, ...
|Known for Hematopoietic Cells | Cell Differentiation | Role Gata1 | Megakaryocytes Mice | Dna Binding|
G Protein-Coupled Bile Acid Receptor TGR5 Activation Inhibits Kidney Disease in Obesity and Diabetes
[ PUBLICATION ]
Obesity and diabetes mellitus are the leading causes of renal disease. In this study, we determined the regulation and role of the G protein-coupled bile acid receptor TGR5, previously shown to be regulated by high glucose and/or fatty acids, in obesity-related glomerulopathy (ORG) and diabetic nephropathy (DN). Treatment of diabetic db/db mice with the selective TGR5 agonist INT-777 decreased proteinuria, podocyte injury, mesangial expansion, fibrosis, and CD68 macrophage infiltration ...
|Known for Kidney Disease | Tgr5 Activation | Bile Acid | Oxidative Stress | Diabetes Obesity|
Expression of advanced glycation end products and their cellular receptor RAGE in diabetic nephropathy and nondiabetic renal disease.
[ PUBLICATION ]
Advanced glycation end products (AGE) contribute to diabetic tissue injury by two major mechanisms, i.e., the alteration of extracellular matrix architecture through nonenzymatic glycation, with formation of protein crosslinks, and the modulation of cellular functions through interactions with specific cell surface receptors, the best characterized of which is the receptor for AGE (RAGE). Recent evidence suggests that the AGE-RAGE interaction may also be promoted by inflammatory ...
|Known for Diabetic Nephropathy | Age Rage | Advanced Glycation | Lupus Nephritis | Messenger Receptor|
Interaction of the RAGE Cytoplasmic Domain with Diaphanous-1 Is Required for Ligand-stimulated Cellular Migration through Activation of Rac1 and Cdc42*
[ PUBLICATION ]
Cellular migration is a fundamental process linked to diverse pathological states such as diabetes and its complications, atherosclerosis, inflammation, and cancer. The receptor for advanced glycation end products (RAGE) is a multiligand cell surface macromolecule which binds distinct ligands that accumulate in these settings. RAGE-ligand interaction evokes central changes in key biological properties of cells, including proliferation, generation of inflammatory mediators, and migration. ...
|Known for Cytoplasmic Domain | Cellular Migration | Rac1 Cdc42 | Binding Protein | Atherosclerosis Diabetes|
Bile acids are ligands for the nuclear hormone receptor farnesoid X receptor (FXR) and the G protein-coupled receptor TGR5. We have shown that FXR and TGR5 have renoprotective roles in diabetes- and obesity-related kidney disease. Here, we determined whether these effects are mediated through differential or synergistic signaling pathways. We administered the FXR/TGR5 dual agonist INT-767 to DBA/2J mice with streptozotocin-induced diabetes, db/db mice with type 2 diabetes, and C57BL/6J ...
|Known for Fxr Tgr5 | Messenger Receptors | Diabetic Mice | Bile Acids | Diabetes Mellitus|
Relevance of different antibody detection methods for the prediction of antibody-mediated rejection and deceased-donor kidney allograft survival
[ PUBLICATION ]
Presensitizing alloantibodies may represent a grave danger in organ transplantation, increasing the risk of antibody-mediated rejection (AMR) and graft loss. However, not all antibodies are harmful to the graft. In our study of a cohort of 325 deceased-donor renal allograft recipients, the patients were determined eligible to receive an allograft based on a negative complement-dependent cytotoxicity (CDC) crossmatch (XM). Yet at the time of transplantation, many candidates displayed ...
|Known for Patients Dsa | Donor Kidney | Transplantation Spa | Graft Survival | Antibody Detection|
Key People For Kidney Injury
Vivette Denise D’Agati:Expert Impact
Concepts for whichVivette Denise D’Agatihas direct influence:Kidney injury, Kidney disease, Nephrotic syndrome, Lupus nephritis, Iga nephropathy, Reperfusion injury, Focal segmental, Renal ischemia.
Vivette Denise D’Agati:KOL impact
Concepts related to the work of other authors for whichfor which Vivette Denise D’Agati has influence:Lupus nephritis, Kidney disease, Nephrotic syndrome, Diabetic nephropathy, Renal function, Oxidative stress, Gene expression.
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