ArticleNature communications2019
SMPDL3b modulates insulin receptor signaling in diabetic kidney disease.
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Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers, 1 of them a synthesis that pooled it.
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78citing papers in PubMed, 1 pooled it
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Who cites it
78 citing papers in PubMed, 1 synthesis or guideline pooled it, 97 citations in OpenAlex.
- Lipid homeostasis in diabetic kidney disease.International journal of biological sciences · 2024Pooled it
- Upregulation of PTPRO by WT1 alleviates podocyte injury in diabetic nephropathy through inhibiting the c-Abl/p53 pathway.Cellular and molecular life sciences : CMLS · 2026Article
- Molecular mechanisms and novel therapeutic targets of diabetic kidney disease.Chinese medical journal · 2026Review
- Ureic clearance granule ameliorates chronic kidney disease by reshaping microbial dysbiosis via modulating bile acid metabolism.Chinese medicine · 2026Article
- Lipid metabolic dysregulation in diabetic kidney disease: mechanisms, cellular impact, and therapeutic strategies.Journal of clinical & translational endocrinology · 2026Review
- Identification and regulatory mechanism analysis of macrophage-related key genes in diabetic nephropathy.Diabetology & metabolic syndrome · 2026Article
- Spatial transcriptomics identifies IL-32 as a lipid droplet-associated cytokine linked to tubular injury in human diabetic kidney disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Protein S-acylation: Pathological mechanisms and novel therapeutic targets for diabetic complications.Chinese herbal medicines · 2026Review
- The lipid-podocyte axis: emerging clues in membranous nephropathy pathogenesis.Frontiers in medicine · 2026Review
- New potential therapeutic targets of metabolic disorder-associated kidney disease and diabetic kidney disease.Kidney international · 2026Review
- Hypoxia-inducible factor 2α overexpression in podocytes ameliorates lipid metabolism disorders in diabetic kidney disease by inhibiting S1P.Renal failure · 2025Article
- Role of nuclear receptors, lipid metabolism, and mitochondrial function in the pathogenesis of diabetic kidney disease.American journal of physiology. Renal physiology · 2025Review
- Circulating Levels of SMPDL3B Define Metabolic Endophenotypes and Subclinical Kidney Alterations in Myalgic Encephalomyelitis.International journal of molecular sciences · 2025Article
- Lipidomics Unveils Critical Lipid Pathway Shifts in Alport Syndrome.Kidney international reports · 2025Article
- PRDM16 deficiency promotes podocyte injury by impairing insulin receptor signaling.Cell death and differentiation · 2025Article
- The enzyme SMPDL3b in podocytes decouples proteinuria from chronic kidney disease progression in experimental Alport Syndrome.Kidney international · 2025Article
- Regulation and function of insulin and insulin-like growth factor receptor signalling.Nature reviews. Molecular cell biology · 2025Review
- Sphingolipid signaling in kidney diseases.American journal of physiology. Renal physiology · 2025Review
- CerS6 links ceramide metabolism to innate immune responses in diabetic kidney disease.Nature communications · 2025Article
- The use of intuitive AF-based modelling for the understanding of activation and signalling through insulin-like receptors.Frontiers in endocrinology · 2025Review
18 more citing papers are in PubMed but not listed here.
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Authors and funding
26 authors at 4 institutions in 6 countries.
A MitrofanovaKatz Family Division of Nephrology and Hypertension, Department of Medicine, University of Miami, Miller School of Medicine, Miami, 33136, FL, USA.
S K MallelaKatz Family Division of Nephrology and Hypertension, Department of Medicine, University of Miami, Miller School of Medicine, Miami, 33136, FL, USA.
G M DucasaKatz Family Division of Nephrology and Hypertension, Department of Medicine, University of Miami, Miller School of Medicine, Miami, 33136, FL, USA.
T H YooKatz Family Division of Nephrology and Hypertension, Department of Medicine, University of Miami, Miller School of Medicine, Miami, 33136, FL, USA.
E Rosenfeld-GurDepartment of Biological Chemistry, Weizmann Institute of Science, Rehovot, 76100, Israel.
I D ZelnikDepartment of Biological Chemistry, Weizmann Institute of Science, Rehovot, 76100, Israel.
J MolinaKatz Family Division of Nephrology and Hypertension, Department of Medicine, University of Miami, Miller School of Medicine, Miami, 33136, FL, USA.
J Varona SantosKatz Family Division of Nephrology and Hypertension, Department of Medicine, University of Miami, Miller School of Medicine, Miami, 33136, FL, USA.
M GeKatz Family Division of Nephrology and Hypertension, Department of Medicine, University of Miami, Miller School of Medicine, Miami, 33136, FL, USA.
A SloanKatz Family Division of Nephrology and Hypertension, Department of Medicine, University of Miami, Miller School of Medicine, Miami, 33136, FL, USA.
J J KimKatz Family Division of Nephrology and Hypertension, Department of Medicine, University of Miami, Miller School of Medicine, Miami, 33136, FL, USA.
C PedigoKatz Family Division of Nephrology and Hypertension, Department of Medicine, University of Miami, Miller School of Medicine, Miami, 33136, FL, USA.
J BrynKatz Family Division of Nephrology and Hypertension, Department of Medicine, University of Miami, Miller School of Medicine, Miami, 33136, FL, USA.
I VolosencoKatz Family Division of Nephrology and Hypertension, Department of Medicine, University of Miami, Miller School of Medicine, Miami, 33136, FL, USA.ORCID http://orcid.org/0000-0003-0580-1811
C FaulKatz Family Division of Nephrology and Hypertension, Department of Medicine, University of Miami, Miller School of Medicine, Miami, 33136, FL, USA.
Y H ZeidanPeggy and Harold Katz Family Drug Discovery Center, University of Miami, Miller School of Medicine, Miami, 33136, FL, USA.
C Garcia HernandezKatz Family Division of Nephrology and Hypertension, Department of Medicine, University of Miami, Miller School of Medicine, Miami, 33136, FL, USA.
A J MendezDiabetes Research Institute, University of Miami, Miller School of Medicine, Miami, 33136, FL, USA.
I LeibigerThe Rolf Luft Research Center for Diabetes and Endocrinology, Karolinska Institutet, Stockholm, 17176, Sweden.
G W BurkeDepartment of Surgery, University of Miami, Miller School of Medicine, Miami, 33136, FL, USA.
A H FutermanDepartment of Biological Chemistry, Weizmann Institute of Science, Rehovot, 76100, Israel.
L BarisoniDepartment of Pathology, University of Miami, Miller School of Medicine, Miami, 33136, FL, USA.
Y IshimotoDivision of Nephrology and Endocrinology, University of Tokyo Graduate School of Medicine, Tokyo, 113-8654, Japan.ORCID http://orcid.org/0000-0001-5773-8637
R InagiDivision of Nephrology and Endocrinology, University of Tokyo Graduate School of Medicine, Tokyo, 113-8654, Japan.ORCID http://orcid.org/0000-0001-7032-7736
S MerscherKatz Family Division of Nephrology and Hypertension, Department of Medicine, University of Miami, Miller School of Medicine, Miami, 33136, FL, USA.
A FornoniKatz Family Division of Nephrology and Hypertension, Department of Medicine, University of Miami, Miller School of Medicine, Miami, 33136, FL, USA. afornoni@med.miami.edu.
University of Miami · USWeizmann Institute of Science · ILThe University of Tokyo · JPKarolinska Institutet · SE
Funding
Coordinating and Bioinformatics Unit for the MMPC/DiaCompU24DK076169 · NIDDK · AUGUSTA UNIVERSITY · PI MCINDOE, RICHARD A. · 2006 to 2018
$42.4MTraining Program in Clinical & Translationa Research in Human Glomerular DiseaseU54DK083912 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI GIPSON, DEBBIE S · 2009 to 2023
$20.3MUniversity of Alabama at Birmingham's Diabetes Research CenterP30DK079626 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI ANANDA BASU · 2013 to 2026
$19.5MMiami Clinical and Translational Science InstituteUL1TR000460 · NCATS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI SACCO, RALPH L. · 2012 to 2016
$16.9MUniversity of Michigan O'Brien Kidney Translational Core CenterP30DK081943 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI BROSIUS, FRANK C · 2008 to 2022
$12.9MCrosstalk Between Lipid Droplets and Other Organelles in PodocytesR01DK104753 · NIDDK · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI FORNONI, ALESSIA · 2015 to 2025
$5.9MPrimary Outcomes in Glomerulonephritis Study (PROGRESS)UM1DK100846 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI HOLZMAN, LAWRENCE B. · 2013 to 2018
$5.8M(PQ12) Targeting SMPDL3b to Prevent Radiation-Induced NephrotoxicityR01CA227493 · NCI · UNIVERSITY OF ROCHESTER · PI MARPLES, BRIAN · 2018 to 2022
$2.0MACTIVATION OF CARDIAC FGFR4 CAUSES LEFT VENTRICULAR HYPERTROPHYR01HL128714 · NHLBI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI FAUL, CHRISTIAN · 2015 to 2019
$1.9MNovel Targets of Rituximab in FSGSR01DK090316 · NIDDK · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI FORNONI, ALESSIA · 2011 to 2015
$1.7MSMPDL3b and podocyte insulin signaling in DKDR01DK117599 · NIDDK · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI FORNONI, ALESSIA · 2018 to 2021
$1.4MThe role of DDR1 in podocyte lipotoxicity and progression of Alport SyndromeF32DK115109 · NIDDK · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI KIM, JINJU · 2017 to 2019
$192kNCATS NIH HHS UL1 TR000460NCI NIH HHS R01 CA227493NHLBI NIH HHS R01 HL128714NIDDK NIH HHS F32 DK115109NIDDK NIH HHS P30 DK079626NIDDK NIH HHS P30 DK081943NIDDK NIH HHS R01 DK090316NIDDK NIH HHS R01 DK104753NIDDK NIH HHS R01 DK117599NIDDK NIH HHS R56 DK104753NIDDK NIH HHS U24 DK076169NIDDK NIH HHS U54 DK083912NIDDK NIH HHS UM1 DK100846
Abstract
Sphingomyelin phosphodiesterase acid-like 3b (SMPDL3b) is a lipid raft enzyme that regulates plasma membrane (PM) fluidity. Here we report that SMPDL3b excess, as observed in podocytes in diabetic kidney disease (DKD), impairs insulin receptor isoform B-dependent pro-survival insulin signaling by interfering with insulin receptor isoforms binding to caveolin-1 in the PM. SMPDL3b excess affects the production of active sphingolipids resulting in decreased ceramide-1-phosphate (C1P) content as observed in human podocytes in vitro and in kidney cortexes of diabetic db/db mice in vivo. Podocyte-specific Smpdl3b deficiency in db/db mice is sufficient to restore kidney cortex C1P content and to protect from DKD. Exogenous administration of C1P restores IR signaling in vitro and prevents established DKD progression in vivo. Taken together, we identify SMPDL3b as a modulator of insulin signaling and demonstrate that supplementation with exogenous C1P may represent a lipid therapeutic strategy to treat diabetic complications such as DKD.
Indexed as
AnimalsAntigens, CDCaveolin 1Cell LineCell MembraneCeramidesCyclic Nucleotide Phosphodiesterases, Type 3Diabetic NephropathiesDisease Models, AnimalFemaleHumansInsulinMaleMiceMice, KnockoutPodocytesAntigens, CDCAV1 protein, humanCav1 protein, mouseCaveolin 1ceramide 1-phosphateCeramidesCyclic Nucleotide Phosphodiesterases, Type 3INSR protein, humanInsulinProtein IsoformsReceptor, InsulinSMPDL3B protein, humansphingomyelinase-like phosphodiesterase 3b, mouseSphingomyelin Phosphodiesterase
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