Podocytes
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Subject Areas on Research
- MYH9 E1841K Mutation Augments Proteinuria and Podocyte Injury and Migration.
- A novel missense mutation of Wilms' Tumor 1 causes autosomal dominant FSGS.
- A novel mouse model of podocyte depletion.
- A proposed taxonomy for the podocytopathies: a reassessment of the primary nephrotic diseases.
- ACE-inhibition increases podocyte number in experimental glomerular disease independent of proliferation.
- APOL1 Nephrotoxicity: What Does Ion Transport Have to Do With It?
- APOL1-G0 or APOL1-G2 Transgenic Models Develop Preeclampsia but Not Kidney Disease.
- APOL1-G0 protects podocytes in a mouse model of HIV-associated nephropathy.
- Activation of Galpha q-coupled signaling pathways in glomerular podocytes promotes renal injury.
- Adriamycin-Induced Podocyte Injury Disrupts the YAP-TEAD1 Axis and Downregulates Cyr61 and CTGF Expression.
- Advances in the biology and genetics of the podocytopathies: implications for diagnosis and therapy.
- Arhgap24 inactivates Rac1 in mouse podocytes, and a mutant form is associated with familial focal segmental glomerulosclerosis.
- Augmenting podocyte injury promotes advanced diabetic kidney disease in Akita mice.
- Beneficial effects of the Rho kinase inhibitor Y27632 in murine puromycin aminonucleoside nephrosis.
- Blockade of the natriuretic peptide clearance receptor attenuates proteinuria in a mouse model of focal segmental glomerulosclerosis.
- COQ6 mutations in human patients produce nephrotic syndrome with sensorineural deafness.
- Calcineurin (CN) activation promotes apoptosis of glomerular podocytes both in vitro and in vivo.
- Cells of renin lineage are progenitors of podocytes and parietal epithelial cells in experimental glomerular disease.
- Collapsing glomerulopathy: an inflammatory podocytopathy?
- Compounds targeting OSBPL7 increase ABCA1-dependent cholesterol efflux preserving kidney function in two models of kidney disease.
- De novo TRIM8 variants impair its protein localization to nuclear bodies and cause developmental delay, epilepsy, and focal segmental glomerulosclerosis.
- Diabetic kidney disease in FVB/NJ Akita mice: temporal pattern of kidney injury and urinary nephrin excretion.
- Dysregulation of WTI (-KTS) is Associated with the Kidney-Specific Effects of the LMX1B R246Q Mutation.
- From man to fish: What can Zebrafish tell us about ApoL1 nephropathy?
- Gq signaling causes glomerular injury by activating TRPC6.
- Gq-dependent signaling upregulates COX2 in glomerular podocytes.
- Guided Differentiation of Mature Kidney Podocytes from Human Induced Pluripotent Stem Cells Under Chemically Defined Conditions.
- IL-1 receptor signaling in podocytes limits susceptibility to glomerular damage.
- Inhibition of p66ShcA longevity gene rescues podocytes from HIV-1-induced oxidative stress and apoptosis.
- Ischemic injury to kidney induces glomerular podocyte effacement and dissociation of slit diaphragm proteins Neph1 and ZO-1.
- Knockout of TRPC6 promotes insulin resistance and exacerbates glomerular injury in Akita mice.
- Losing their footing: Rac1 signaling causes podocyte detachment and FSGS.
- Mechanisms of the proteinuria induced by Rho GTPases.
- Mutations in the gene that encodes the F-actin binding protein anillin cause FSGS.
- Notch signaling: a common pathway of injury in podocytopathies?
- Pathogenesis and therapy of focal segmental glomerulosclerosis: an update.
- Phosphodiesterase 5 inhibition ameliorates angiontensin II-induced podocyte dysmotility via the protein kinase G-mediated downregulation of TRPC6 activity.
- Podocyte biology in segmental sclerosis and progressive glomerular injury.
- Podocyte density is reduced in kidney allografts with high-risk APOL1 genotypes at transplantation.
- Podocyte effacement closely links to suPAR levels at time of posttransplantation focal segmental glomerulosclerosis occurrence and improves with therapy.
- Podocyte-specific knockout of cyclooxygenase 2 exacerbates diabetic kidney disease.
- RNA sequencing of isolated cell populations expressing human APOL1 G2 risk variant reveals molecular correlates of sickle cell nephropathy in zebrafish podocytes.
- Rare hereditary COL4A3/COL4A4 variants may be mistaken for familial focal segmental glomerulosclerosis.
- Reduction of Stat3 activity attenuates HIV-induced kidney injury.
- Regulation of cofilin phosphorylation in glomerular podocytes by testis specific kinase 1 (TESK1).
- Revisiting the determinants of the glomerular filtration barrier: what goes round must come round.
- SMPDL3b modulates insulin receptor signaling in diabetic kidney disease.
- Special deLIVERy: podocyte injury promotes renal angiotensin II generation from liver-derived angiotensinogen.
- Steroid-sensitive nephrotic syndrome candidate gene CLVS1 regulates podocyte oxidative stress and endocytosis.
- Stressed-out podocytes in diabetes?
- TNFR2 interposes the proliferative and NF-κB-mediated inflammatory response by podocytes to TNF-α.
- TRPC6 enhances angiotensin II-induced albuminuria.
- The Bowman's shield: a tribute to translational science and Detlef Schlöndorff.
- The EP4 receptor for prostaglandin E2 in glomerular disease: a good receptor turned bad?
- The Human FSGS-Causing ANLN R431C Mutation Induces Dysregulated PI3K/AKT/mTOR/Rac1 Signaling in Podocytes.
- The homophilic adhesion molecule sidekick-1 contributes to augmented podocyte aggregation in HIV-associated nephropathy.
- The inducible deletion of Drosha and microRNAs in mature podocytes results in a collapsing glomerulopathy.
- The kd/kd mouse is a model of collapsing glomerulopathy.
- Therapeutic targets in focal and segmental glomerulosclerosis.
- Transactivation of the epidermal growth factor receptor by angiotensin II in glomerular podocytes.
- Translating genetic findings in hereditary nephrotic syndrome: the missing loops.
- Twist1 in podocytes ameliorates podocyte injury and proteinuria by limiting CCL2-dependent macrophage infiltration.
- Ultrastructural Characterization of Proteinuric Patients Predicts Clinical Outcomes.
- Unexpected role of TRPC6 channel in familial nephrotic syndrome: does it have clinical implications?
- Urinary Single-Cell Profiling Captures the Cellular Diversity of the Kidney.
- VEGF inhibition and renal thrombotic microangiopathy.
- VEGF inhibition and renal thrombotic microangiopathy.
- Wnt/β-catenin pathway in podocytes integrates cell adhesion, differentiation, and survival.
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Keywords of People
- Sparks, Matthew A., Associate Professor of Medicine, Medicine, Nephrology