Professor in Pediatrics-Kidney Diseases
Pediatric Nephrology
Dr. Howard W. Schnaper, MD
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Dr. Howard W. Schnaper is an expert in the field of Pediatric Nephrology. He went to University of Maryland School of Medicine. University of Maryland School of Medicine is ranked 37 in research and 52 in primary care medicine Howard Schnaper has written publications. He has 98 publications published with PubMed. The lastest paper is: 'Cell signal transduction through the mitogen-activated protein kinase pathway.'
Publications
- Defining new surrogate markers for CKD progression.
- Epidermal growth factor inhibits transforming growth factor-β-induced fibrogenic differentiation marker expression through ERK activation.
- Hypoxia-inducible factor-2α and TGF-β signaling interact to promote normoxic glomerular fibrogenesis.
- Serine-204 in the Linker Region of Smad3 Mediates the Collagen-I Response to TGF-β in a Cell Phenotype-Specific Manner.
- Remnant nephron physiology and the progression of chronic kidney disease.
- Divergent roles of Smad3 and PI3-kinase in murine adriamycin nephropathy indicate distinct mechanisms of proteinuria and fibrogenesis.
- Talking at cross purposes: molecular interactions downstream from TGF-beta.
- Risk factors for cardiovascular disease in children on maintenance dialysis.
- Antithrombin III, protein S, and coagulation in the nephrotic syndrome.
- Sp1 and Smad proteins cooperate to mediate transforming growth factor-beta 1-induced alpha 2(I) collagen expression in human glomerular mesangial cells.
- Shear stress enhances human endothelial cell wound closure in vitro.
- Signal transduction through protein kinase C.
- Sex steroids and the endothelium.
- TGF-beta1 activates MAP kinase in human mesangial cells: a possible role in collagen expression.
- The transforming growth factor-beta/SMAD signaling pathway is present and functional in human mesangial cells.
- Reflections on the pediatric chief residency.
- Estrogen: it's not just for reproduction any more.
- Angiostatin binds ATP synthase on the surface of human endothelial cells.
- Cell signal transduction through the mitogen-activated protein kinase pathway.
- Basic fibroblast growth factor release by human coronary artery endothelial cells is enhanced by matrix proteins, 17beta-estradiol, and a PKC signaling pathway.
- Regulation of human mesangial cell collagen expression by transforming growth factor-beta1.
- Estrogen stimulates delayed mitogen-activated protein kinase activity in human endothelial cells via an autocrine loop that involves basic fibroblast growth factor.
- The nephrotic syndrome: from the simple to the complex.
- Oestrogen and endothelial cell angiogenic activity.
- Increased expression of extracellular matrix proteins and decreased expression of matrix proteases after serial passage of glomerular mesangial cells.
- Human prostate carcinoma cells express enzymatic activity that converts human plasminogen to the angiogenesis inhibitor, angiostatin.
- Early markers of ventilator-induced lung injury in rats.
- Integrin receptors, the cytoskeleton, and glomerular cell function.
- Expression of an estrogen receptor by human coronary artery and umbilical vein endothelial cells.
- Primary nephrotic syndrome of childhood.
- Basement membrane matrices in tissue development.
- The laminins: a family of basement membrane glycoproteins important in cell differentiation and tumor metastases.
- Regulation of cell function by extracellular matrix.
- Role of laminin in endothelial cell recognition and differentiation.
- The endothelium as an immune organ: studies of endothelial-leukocyte interactions.
- Type IV collagenase(s) and TIMPs modulate endothelial cell morphogenesis in vitro.
- 12-O-tetradecanoylphorbol 13-acetate stimulates human T-lymphocyte adherence to the fibronectin RGD domain and the laminin IKVAV domain.
- Human T lymphocytes synthesize the 92 kDa type IV collagenase (gelatinase B).
- Immunization practices in childhood nephrotic syndrome: a survey of North American pediatric nephrologists.
- Call for a registry of complications of immunization in nephrotic children!
- Apoptosis: death as a "vital" biological function.
- Balance between matrix synthesis and degradation: a determinant of glomerulosclerosis.
- Plasminogen activators augment endothelial cell organization in vitro by two distinct pathways.
- ECM degradation by cultured human mesangial cells is mediated by a PA/plasmin/MMP-2 cascade.
- Estrogen promotes angiogenic activity in human umbilical vein endothelial cells in vitro and in a murine model.
- HIV-1 infection alters monocyte interactions with human microvascular endothelial cells.
- Estradiol enhances leukocyte binding to tumor necrosis factor (TNF)-stimulated endothelial cells via an increase in TNF-induced adhesion molecules E-selectin, intercel...
- Cerebral cortical atrophy in pediatric patients with end-stage renal disease.
- Identification and initial characterization of concanavalin A- and interferon-induced human suppressor factors: evidence for a human equivalent of murine soluble immun...
- Suppressor T cell activation by human leukocyte interferon.
- Identification of the lymphokine soluble immune response suppressor in urine of nephrotic children.
- Cystinosis presenting with features suggesting Bartter syndrome. Case report and literature review.
- Soluble immune response suppressor (SIRS).
- Steroid-sensitive mechanism of soluble immune response suppressor production in steroid-responsive nephrotic syndrome.
- Immunology.
- Suppression of immune responses to sheep erythrocytes by the lymphokine soluble immune response suppressor (SIRS) in vivo.
- Prolonged survival in a child with renovascular hypertension from abdominal-pulmonary Takayasu''s arteritis.
- The immune system in minimal change nephrotic syndrome.
- Immunology. Active participation by visceral tissue in the immune response.
- The soluble immune response suppressor pathway in nephrotic syndrome.
- Divalent metal requirement for soluble immune response suppressor (SIRS) activity.
- A role for histamine type II (H-2) receptor binding in production of the lymphokine, soluble immune response suppressor (SIRS).
- Inhibition of interleukin 1 (IL-1)-elicited leukocytosis and LPS-induced fever by soluble immune response suppressor (SIRS).
- Immunology. Regulation of cellular function at tissue, hormonal and molecular levels.
- Putative N-terminal sequence of murine soluble immune response suppressor (SIRS): significant homology with short neurotoxin 1.
- Immunological mediators and glomerular cell function.
- Steroid-dependent nephrotic syndrome following renal transplantation for congenital nephrotic syndrome.
- Control of interleukin 1 (IL-1) activity. I. Inhibition of IL-1 activity by soluble immune response suppressor (SIRS) in vitro.
- A regulatory system for soluble immune response suppressor production in steroid-responsive nephrotic syndrome.
- Hormonal mediators of immune function: new targets for therapeutic intervention.
- Early occurrence of end-stage renal disease in a patient with infantile nephropathic cystinosis.
- Euthanasia: is there an answer?
- Euthanasia: an overview.
- An assessment of adverse effects of methyldopa and propranolol.
- Chlorthalidone and serum cholesterol.
- Use of paramedical personnel in routine antihypertensive treatment.
- Estradiol enhances endothelial cell interactions with extracellular matrix proteins via an increase in integrin expression and function.
- High ambient glucose enhances sensitivity to TGF-beta1 via extracellular signal--regulated kinase and protein kinase Cdelta activities in human mesangial cells.
- The phosphatidylinositol 3-kinase/Akt pathway enhances Smad3-stimulated mesangial cell collagen I expression in response to transforming growth factor-beta1.
- Interdependence of HIF-1? and TGF-?/Smad3 signaling in normoxic and hypoxic renal epithelial cell collagen expression.
- Loss of beta1-integrin enhances TGF-beta1-induced collagen expression in epithelial cells via increased alphavbeta3-integrin and Rac1 activity.
- A conceptual framework for the molecular pathogenesis of progressive kidney disease.
- Rac1 promotes TGF-beta-stimulated mesangial cell type I collagen expression through a PI3K/Akt-dependent mechanism.
- Role of SARA (SMAD anchor for receptor activation) in maintenance of epithelial cell phenotype.
- Progression of glomerular and tubular disease in pediatrics.
- TGF-beta signal transduction in chronic kidney disease.
- High ambient glucose augments angiotensin II-induced proinflammatory gene mRNA expression in human mesangial cells: effects of valsartan and simvastatin.
- Advances in the biology and genetics of the podocytopathies: implications for diagnosis and therapy.
- MAP-kinase activity necessary for TGFbeta1-stimulated mesangial cell type I collagen expression requires adhesion-dependent phosphorylation of FAK tyrosine 397.
- A proposed taxonomy for the podocytopathies: a reassessment of the primary nephrotic diseases.
- The creation of the Council of Pediatric Subspecialties: addressing the needs of the subspecialties and subspecialists.
- Cell phenotype-specific down-regulation of Smad3 involves decreased gene activation as well as protein degradation.
- RACK1 binds to Smad3 to modulate transforming growth factor-beta1-stimulated alpha2(I) collagen transcription in renal tubular epithelial cells.
- TGF-beta receptor-binding proteins: complex interactions.
- Why kidneys fail: report from an American Society of Nephrology Advances in Research Conference.
- Renal fibrosis.
- Renal endowment: developmental origins of adult disease.
Schools
University Of Maryland School Of Medicine
Mt Sinai Hospital
Wash University School Med
Doctors Specialties
- Pediatric Nephrology
Accepted Insurances
Education
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Mount Sinai School of Medicine -
University of Maryland School of Medicine
Hospital
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Lurie Children's Hospital of Chicago -
Northwestern Memorial Hospital
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