ArticleDiabetologia2011
C-reactive protein promotes diabetic kidney disease in a mouse model of type 1 diabetes.
Article in Diabetologia, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 74 citations in OpenAlex.
- Serum C-reactive protein and C-reactive protein derived markers in diabetic microvascular complications.World journal of diabetes · 2025Review
- Effectiveness and safety of Tongxinluo capsule for diabetic kidney disease: A systematic review and meta-analysis.World journal of diabetes · 2025Article
- C-reactive protein promotes diabetic kidney disease via Smad3-mediated NLRP3 inflammasome activation.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- The Renal Micro-Vasculopathy and Systemic Aldosterone-Renin Ratio (ARR) in Type 2 Diabetic Patients-A Retrospective Real-World Study.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Article
- Stroke-Induced Renal Dysfunction: Underlying Mechanisms and Challenges of the Brain-Kidney Axis.CNS neuroscience & therapeutics · 2024Review
- Evaluation of serum vitamin D metabolites, phagocytosis, and biomarkers of inflammation in dogs with naturally occurring diabetes mellitus.Frontiers in veterinary science · 2024Article
- [The Role of TGF-β1/SMAD in Diabetic Nephropathy: Mechanisms and Research Development].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2023Article
- Role of C-Reactive Protein in Kidney Diseases.Kidney diseases (Basel, Switzerland) · 2023Review
- Association of high-sensitivity C-reactive protein and diabetic nephropathy in patients with type 2 diabetes: a Mendelian randomization study.BMJ open diabetes research & care · 2023Observational
- Secretory quality control constrains functional selection-associated protein structure innovation.Communications biology · 2022Article
- What do we actually know about exosomal microRNAs in kidney diseases?Frontiers in physiology · 2022Review
- Smad3 Signatures in Renal Inflammation and Fibrosis.International journal of biological sciences · 2022Review
- The Macrophage Iron Signature in Health and Disease.International journal of molecular sciences · 2021Review
- DPP4/CD32b/NF-κB Circuit: A Novel Druggable Target for Inhibiting CRP-Driven Diabetic Nephropathy.Molecular therapy : the journal of the American Society of Gene Therapy · 2021Article
- Bioinformatics analysis of genes related to iron death in diabetic nephropathy through network and pathway levels based approaches.PloS one · 2021Article
- Deletion of Smad3 protects against C-reactive protein-induced renal fibrosis and inflammation in obstructive nephropathy.International journal of biological sciences · 2021Article
- Latent TGF-β1 protects against diabetic kidney disease via Arkadia/Smad7 signaling.International journal of biological sciences · 2021Article
- Epigenetics and Inflammation in Diabetic Nephropathy.Frontiers in physiology · 2021Review
- The varying roles of macrophages in kidney injury and repair.Current opinion in nephrology and hypertension · 2020Review
- Accelerated Kidney Aging in Diabetes Mellitus.Oxidative medicine and cellular longevity · 2020Review
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisAlthough C-reactive protein (CRP) has been implicated as a risk factor in diabetes, its pathogenic importance in diabetic kidney disease (DKD) remains unclear. The present study investigated the potential role of CRP in DKD.
methodsDiabetes was induced by streptozotocin in human CRP transgenic and wild-type mice for assessment of kidney injury at 24 weeks by real-time PCR, immunohistochemistry and western blot analysis. In vitro, the pathogenic effect of CRP was investigated using human kidney tubular epithelial cells cultured with high glucose and/or CRP.
resultsWe found that CRP transgenic mice developed much more severe diabetic kidney injury than wild-type mice, as indicated by a significant increase in urinary albumin excretion and kidney injury molecule-1 abundance, enhanced infiltration of macrophages and T cells, and upregulation of pro-inflammatory cytokines (IL-1β, TNFα) and extracellular matrix (collagen I, III and IV). Enhanced renal inflammation and fibrosis in CRP transgenic mice was associated with upregulation of CRP receptor, CD32a, and over-activation of the TGF-β/SMAD and nuclear factor κB signalling pathways. In vitro, CRP significantly upregulated pro-inflammatory cytokines (IL-1β, TNFα, monocyte chemoattractant protein-1 [MCP-1]) and pro-fibrotic growth factors (TGF-β1, connective tissue growth factor [CTGF]) via CD32a/64. CRP was induced by high glucose, which synergistically promoted high glucose-mediated renal inflammation and fibrosis. CONCLUSIONS/
interpretationCRP is not only a biomarker, but also a mediator in DKD. Enhanced activation of TGF-β/SMAD and nuclear factor κB signalling pathways may be the mechanisms by which CRP promotes renal inflammation and fibrosis under diabetic conditions.
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