Simona Buelli

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Fractalkine and CX3CR1 Mediate Leukocyte Capture by Endothelium in Response to Shiga Toxin1

G. Remuzzi, M. Morigi, C. Zoja, 2008, The Journal of Immunology.

Shiga toxin-associated hemolytic uremic syndrome: pathophysiology of endothelial dysfunction

M. Morigi, C. Zoja, Simona Buelli, 2010, Pediatric Nephrology.

Mitochondrial-dependent Autoimmunity in Membranous Nephropathy of IgG4-related Disease

G. Remuzzi, A. Benigni, M. Kawano, 2015, EBioMedicine.

Sirtuin3 Dysfunction Is the Key Determinant of Skeletal Muscle Insulin Resistance by Angiotensin II

N. Perico, G. Remuzzi, A. Benigni, 2015, PloS one.

Protein overload-induced NF-kappaB activation in proximal tubular cells requires H(2)O(2) through a PKC-dependent pathway.

G. Remuzzi, M. Morigi, C. Zoja, 2002, Journal of the American Society of Nephrology : JASN.

Effects of MCP-1 Inhibition by Bindarit Therapy in a Rat Model of Polycystic Kidney Disease

N. Perico, G. Remuzzi, A. Remuzzi, 2014, Nephron.

β-arrestin-1 drives endothelin-1-mediated podocyte activation and sustains renal injury.

G. Remuzzi, A. Benigni, E. Gagliardini, 2014, Journal of the American Society of Nephrology : JASN.

Protein overload induces fractalkine upregulation in proximal tubular cells through nuclear factor kappaB- and p38 mitogen-activated protein kinase-dependent pathways.

G. Remuzzi, A. Benigni, M. Abbate, 2003, Journal of the American Society of Nephrology : JASN.

Shiga Toxin Capture by Endothelium in Response to Fractalkine and CX3CR1 Mediate Leukocyte

G. Remuzzi, M. Morigi, C. Zoja, 2008 .

SGLT2 inhibitor dapagliflozin limits podocyte damage in proteinuric nondiabetic nephropathy.

G. Remuzzi, A. Benigni, M. Morigi, 2018, JCI insight.

Untangling the Knot in Diabetic Nephropathy: The Unanticipated Role of Glycocalyx in the Antiproteinuric Effect of Endothelin Receptor Antagonists

A. Benigni, Luca Perico, Simona Buelli, 2016, Diabetes.

Endothelin-targeted new treatments for proteinuric and inflammatory glomerular diseases: focus on the added value to anti-renin-angiotensin system inhibition

A. Benigni, D. Kohan, Simona Buelli, 2020, Pediatric Nephrology.

Proteasomal processing of albumin by renal dendritic cells generates antigenic peptides.

G. Remuzzi, A. Benigni, R. Fanelli, 2009, Journal of the American Society of Nephrology : JASN.

Permselective dysfunction of podocyte-podocyte contact upon angiotensin II unravels the molecular target for renoprotective intervention.

G. Remuzzi, A. Remuzzi, M. Abbate, 2006, The American journal of pathology.

Microvascular Thrombosis Exuberant C3a Formation That Triggers Complement by Shiga Toxin Promotes Alternative Pathway Activation of

G. Remuzzi, M. Gobbi, M. Morigi, 2011 .

Activation of porcine endothelium in response to xenogeneic serum causes thrombosis independently of platelet activation

G. Remuzzi, M. Morigi, D. Macconi, 2005, Xenotransplantation.

Shiga Toxin 2 Triggers C3a-Dependent Glomerular and Tubular Injury through Mitochondrial Dysfunction in Hemolytic Uremic Syndrome

G. Remuzzi, A. Benigni, B. Imberti, 2022, Cells.

MYO1E mutations and childhood familial focal segmental glomerulosclerosis.

G. Remuzzi, F. Macciardi, A. Benigni, 2011, The New England journal of medicine.

Angiotensin II contributes to diabetic renal dysfunction in rodents and humans via Notch1/Snail pathway.

N. Perico, G. Remuzzi, A. Benigni, 2013, The American journal of pathology.

A previously unrecognized role of C3a in proteinuric progressive nephropathy

G. Remuzzi, A. Benigni, C. Rota, 2016, Scientific Reports.

Complement Activation Contributes to the Pathophysiology of Shiga Toxin-Associated Hemolytic Uremic Syndrome

G. Remuzzi, M. Morigi, C. Zoja, 2019, Microorganisms.

Shiga toxin triggers endothelial and podocyte injury: the role of complement activation

M. Morigi, C. Zoja, Simona Buelli, 2019, Pediatric Nephrology.

Alternative Pathway Activation of Complement by Shiga Toxin Promotes Exuberant C3a Formation That Triggers Microvascular Thrombosis

G. Remuzzi, M. Gobbi, M. Morigi, 2011, The Journal of Immunology.

In response to protein load podocytes reorganize cytoskeleton and modulate endothelin-1 gene: implication for permselective dysfunction of chronic nephropathies.

G. Remuzzi, A. Benigni, M. Morigi, 2005, The American journal of pathology.

Shiga toxin promotes podocyte injury in experimental hemolytic uremic syndrome via activation of the alternative pathway of complement.

G. Remuzzi, J. Thurman, M. Morigi, 2014, Journal of the American Society of Nephrology : JASN.

Membranous nephropathy associated with IgG4-related disease.

G. Remuzzi, V. D’Agati, D. Salant, 2011, American journal of kidney diseases : the official journal of the National Kidney Foundation.

Protein Overload-Induced NF-κB Activation in Proximal Tubular Cells Requires H2O2 through a PKC-Dependent Pathway

G. Remuzzi, M. Morigi, C. Zoja, 2002 .

C3a receptor blockade protects podocytes from injury in diabetic nephropathy.

G. Remuzzi, A. Benigni, M. Morigi, 2020, JCI insight.

Endothelin in chronic proteinuric kidney disease.

A. Benigni, E. Gagliardini, Simona Buelli, 2011, Contributions to nephrology.

Protein load impairs factor H binding promoting complement-dependent dysfunction of proximal tubular cells.

G. Remuzzi, P. Zipfel, M. Abbate, 2009, Kidney international.

Shigatoxin-induced endothelin-1 expression in cultured podocytes autocrinally mediates actin remodeling.

G. Remuzzi, A. Benigni, M. Morigi, 2006, The American journal of pathology.