ArticleJCI insight2022
Deficiency of CFB attenuates renal tubulointerstitial damage by inhibiting ceramide synthesis in diabetic kidney disease.
Article in JCI insight, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 30 citations in OpenAlex.
- Targeting ceramides in metabolic syndrome: recent advances and therapeutic opportunities.Acta diabetologica · 2026Review
- Molecular mechanisms and novel therapeutic targets of diabetic kidney disease.Chinese medical journal · 2026Review
- Molecular mechanisms and therapeutic strategies of glomerular cell senescence in diabetic kidney disease: from heterogeneity to precision intervention.Cellular and molecular life sciences : CMLS · 2026Review
- Dapagliflozin induces renal lipidomic remodeling and systemic metabolic improvement.Biology direct · 2026Article
- Complement Dysregulation in Kidney Diseases: Mechanisms, Biomarkers, and Emerging Targeted Therapies.International journal of molecular sciences · 2026Review
- Lifestyles, metabolome and diabetic kidney disease: a cohort study.QJM : monthly journal of the Association of Physicians · 2026Article
- Complement 5a receptor 2 attenuates diabetic kidney disease by promoting mitochondria-associated endoplasmic reticulum membrane formation mediated by PSS-MFN2 interaction.Cell discovery · 2026Article
- Feasibility of Integrating Urinary Proteomics and Machine Learning for Diagnosing Diabetic Nephropathy.Journal of proteome research · 2026Article
- Neuroinflammatory Mechanisms and Therapeutic Targets in Oxaliplatin-Induced Peripheral Neuropathy: a Comprehensive Review.Neurotoxicity research · 2025Review
- Progress in the study of the role of C5a-induced tubular cell senescence in the progression of diabetic kidney disease.Annals of medicine · 2025Review
- Aucubin ameliorates diabetic kidney disease by restoring hGENCs autophagy through promoting phosphorylation of ATG4B protein.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
- Complement anaphylatoxins: Potential therapeutic target for diabetic kidney disease.Diabetic medicine : a journal of the British Diabetic Association · 2025Review
- Complement classical and alternative pathway activation contributes to diabetic kidney disease progression: a glomerular proteomics on kidney biopsies.Scientific reports · 2025Article
- Identification and validation of prognostic genes associated with T-cell exhaustion and macrophage polarization in breast cancer.Frontiers in endocrinology · 2025Article
- Targeting lipid metabolic reprogramming to alleviate diabetic kidney disease: molecular insights and therapeutic strategies.Frontiers in immunology · 2025Review
- Programmed Cell Death in Diabetic Kidney Disease: Mechanisms and Therapeutic Targeting.Journal of inflammation research · 2025Review
- Complement factor B inhibitor LNP023 mediates the effect and mechanism of AMPK/mTOR on autophagy and oxidative stress in lupus nephritis.The Kaohsiung journal of medical sciences · 2024Article
- Apical tubular complement activation and the loss of kidney function in proteinuric kidney diseases.Clinical kidney journal · 2024Review
- Targeting EphA2: a promising strategy to overcome chemoresistance and drug resistance in cancer.Journal of molecular medicine (Berlin, Germany) · 2024Review
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Accumulating evidence suggests the pathogenic role of immunity and metabolism in diabetic kidney disease (DKD). Herein, we aimed to investigate the effect of complement factor B (CFB) on lipid metabolism in the development of DKD. We found that in patients with diabetic nephropathy, the staining of Bb, CFB, C3a, C5a, and C5b-9 was markedly elevated in renal tubulointerstitium. Cfb-knockout diabetic mice had substantially milder tubulointerstitial injury and less ceramide biosynthesis. The in vitro study demonstrated that cytokine secretion, endoplasmic reticulum stress, oxidative stress, and cell apoptosis were ameliorated in HK-2 cells transfected with siRNA of CFB under high-glucose conditions. Exogenous ceramide supplementation attenuated the protective effect of CFB knockdown in HK-2 cells, while inhibiting ceramide synthases (CERS) with fumonisin B1 in CFB-overexpressing cells rescued the cell injury. CFB knockdown could downregulate the expression of NF-κB p65, which initiates the transcription of CERS3. Furthermore, C3 knockdown abolished CFB-mediated cytokine secretion, NF-κB signaling activation, and subsequently ceramide biosynthesis. Thus, CFB deficiency inhibited activation of the complement alternative pathway and attenuated kidney damage in DKD, especially tubulointerstitial injury, by inhibiting the NF-κB signaling pathway, further blocking the transcription of CERS, which regulates the biosynthesis of ceramide. CFB may be a promising therapeutic target of DKD.
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