ArticleThe Journal of clinical investigation2018
CaMK4 compromises podocyte function in autoimmune and nonautoimmune kidney disease.
Article in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed, 115 citations in OpenAlex.
- The Human PNPLA3FASEB bioAdvances · 2026Article
- IgG Glycosylation-Dependent CLEC7A Signaling Drives Podocyte Dysfunction in Lupus Nephritis.Arthritis & rheumatology (Hoboken, N.J.) · 2026Article
- Targeting FcRn for immunomodulation: a promising therapy in autoimmune inflammatory rheumatic diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Cell-Targeted Inhibition of CaMK4 Suppresses Tertiary Lymphoid-like Structure Development in Lupus-Prone Mice.International journal of molecular sciences · 2026Article
- Remodeling the Inflammatory Microenvironment: Nanomaterial-Based Targeted Strategies for Systemic Lupus Erythematosus and Lupus Nephritis.Small science · 2026Review
- Glucose metabolic reprogramming in systemic lupus erythematosus and lupus nephritis: theoretical foundations and therapeutic implications.Frontiers in immunology · 2026Review
- Immune podocyte injury in autoimmune glomerular diseases.Frontiers in immunology · 2026Review
- Multi-cellular network model predicts alterations in glomerular endothelial structure in diabetic kidney disease.PLoS computational biology · 2025Article
- Urine proteins reveal distinct coagulation and complement cascades underlying acute versus chronic lupus nephritis.The Journal of clinical investigation · 2025Article
- Aberrant Glycosylation of IgG in Children With Active Lupus Nephritis Alters Podocyte Metabolism and Causes Podocyte Injury.Arthritis & rheumatology (Hoboken, N.J.) · 2025Article
- Glycosylation in kidney diseases.Precision clinical medicine · 2025Review
- The CaPediatric nephrology (Berlin, Germany) · 2025Review
- Dysregulated Anaerobic Glycolysis in Podocytes is Relevant to the Progression of Focal Segmental Glomerulosclerosis.Kidney international reports · 2025Article
- Kidney immunology from pathophysiology to clinical translation.Nature reviews. Immunology · 2025Review
- Screening and Identification of Novel DNA Aptamer for Targeted Delivery to Injured Podocytes in Glomerular Diseases.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Nanotherapeutics in Kidney Disease: Innovations, Challenges, and Future Directions.Journal of the American Society of Nephrology : JASN · 2025Review
- Calcium calmodulin kinase IV deficiency in podocytes prevents the development of lupus nephritis.Clinical immunology (Orlando, Fla.) · 2025Article
- Hypoxia Promotes the Expression of ADAM9 by Tubular Epithelial Cells, Which Enhances Transforming Growth Factor β1 Activation and Promotes Tissue Fibrosis in Patients With Lupus Nephritis.Arthritis & rheumatology (Hoboken, N.J.) · 2025Article
- Podocyte, tubular epithelial-immune cell interplay in the pathogenesis of lupus nephritis.Frontiers in immunology · 2025Review
- The Role of Podocytes in Lupus Pathology.Current rheumatology reports · 2024Review
4 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
14 authors at 6 institutions in 2 countries.
Funding
Abstract
Podocyte malfunction occurs in autoimmune and nonautoimmune kidney disease. Calcium signaling is essential for podocyte injury, but the role of Ca2+/calmodulin-dependent kinase (CaMK) signaling in podocytes has not been fully explored. We report that podocytes from patients with lupus nephritis and focal segmental glomerulosclerosis and lupus-prone and lipopolysaccharide- or adriamycin-treated mice display increased expression of CaMK IV (CaMK4), but not CaMK2. Mechanistically, CaMK4 modulated podocyte motility by altering the expression of the GTPases Rac1 and RhoA and suppressed the expression of nephrin, synaptopodin, and actin fibers in podocytes. In addition, it phosphorylated the scaffold protein 14-3-3β, which resulted in the release and degradation of synaptopodin. Targeted delivery of a CaMK4 inhibitor to podocytes preserved their ultrastructure, averted immune complex deposition and crescent formation, and suppressed proteinuria in lupus-prone mice and proteinuria in mice exposed to lipopolysaccharide-induced podocyte injury by preserving nephrin/synaptopodin expression. In animals exposed to adriamycin, podocyte-specific delivery of a CaMK4 inhibitor prevented and reversed podocyte injury and renal disease. We conclude that CaMK4 is pivotal in immune and nonimmune podocyte injury and that its targeted cell-specific inhibition preserves podocyte structure and function and should have therapeutic value in lupus nephritis and podocytopathies, including focal segmental glomerulosclerosis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.