ArticleThe American journal of pathology2011
Loss of endogenous bone morphogenetic protein-6 aggravates renal fibrosis.
Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 60 citations in OpenAlex.
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- Cardiometabolic protein expression levels and pathways associated with kidney function decline in older European adults with advanced kidney disease.Clinical kidney journal · 2025Article
- Bone morphogenetic protein 6 (BMP6) antagonises experimental proliferative vitreoretinopathy established by TGF-β2 stimulation in retinal pigment epithelial cells through modulation of the p38 and JNK MAPK pathways.Cell and tissue research · 2024Article
- Genetic association and transferability for urinary albumin-creatinine ratio as a marker of kidney disease in four Sub-Saharan African populations and non-continental individuals of African ancestry.Frontiers in genetics · 2024Article
- Circulating extracellular vesicles in human cardiorenal syndrome promote renal injury in a kidney-on-chip system.JCI insight · 2023Article
- Stem cell pathology: histogenesis of malignant fibrous histiocytoma and characterization of myofibroblasts appearing in fibrotic lesions.The Journal of veterinary medical science · 2023Review
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- Identification of Genetic Markers Linked to The Activity of Indoleamine 2,3-Dioxygenase and Kidney Function.Metabolites · 2023Article
- Distinctive modulation of hepcidin in cancer and its therapeutic relevance.Frontiers in oncology · 2023Review
- Neuroblastoma suppressor of tumorigenicity 1 is a circulating protein associated with progression to end-stage kidney disease in diabetes.Science translational medicine · 2022Article
- Mapping the single-cell transcriptomic response of murine diabetic kidney disease to therapies.Cell metabolism · 2022Article
- Modeling injury and repair in kidney organoids reveals that homologous recombination governs tubular intrinsic repair.Science translational medicine · 2022Article
- Investigating the Molecular Mechanisms of Renal Hepcidin Induction and Protection upon Hemoglobin-Induced Acute Kidney Injury.International journal of molecular sciences · 2022Article
- Genome-wide identification, characterization and expression analysis of the BMP family associated with beak-like teeth inFrontiers in genetics · 2022Article
- Bone Morphogenetic Proteins (BMPs), Extracellular Matrix Metalloproteinases Inducer (EMMPRIN), and Macrophage Migration Inhibitory Factor (MIF): Usefulness in the Assessment of Tubular Dysfunction Related to Chronic Kidney Disease (CKD).Journal of clinical medicine · 2021Article
- Candidate rejuvenating factor GDF11 and tissue fibrosis: friend or foe?GeroScience · 2020Review
- TGF-β Pathway in Salivary Gland Fibrosis.International journal of molecular sciences · 2020Review
- The Role of Bone Morphogenetic Proteins in Diabetic Complications.ACS pharmacology & translational science · 2020Review
- Genome-wide comparative analysis ofbone morphogenetic proteins: genomic structure, phylogeny, and expression patterns in the golden pompano,Trachinotus ovatus(Linnaeus, 1758).Fish physiology and biochemistry · 2020Article
- Bone morphogenetic protein 6 (BMP-6) modulates lung function, pulmonary iron levels and cigarette smoke-induced inflammation.Mucosal immunology · 2019Article
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10 authors at 3 institutions in 2 countries.
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No grant is acknowledged in the PubMed record.
Abstract
Bone morphogenetic protein-6 (BMP-6) suppresses inflammatory genes in renal proximal tubular cells and regulates iron metabolism by inducing hepcidin. In diabetic patients, an increase of myofibroblast progenitor cells (MFPCs), also known as fibrocytes, was found to be associated with decreased BMP-6 expression. We hypothesized that loss of endogenous BMP-6 would aggravate renal injury and fibrosis. Wild type (WT) and BMP-6 null mice underwent unilateral ureteral obstruction. In WT mice, ureteral obstruction down-regulated BMP-6. Obstructed kidneys of BMP-6 null mice showed more casts (1.5-fold), epithelial necrosis (1.4-fold), and brush border loss (1.3-fold). This was associated with more inflammation (1.8-fold more CD45(+) cells) and more pronounced overexpression of profibrotic genes for αSMA (2.0-fold), collagen I (6.8-fold), fibronectin (4.3-fold), CTGF (1.8-fold), and PAI-1 (3.8-fold), despite similar BMP-7 expression. Also, 1.3-fold more MFPCs were obtained from BMP-6 null than from WT mononuclear cell cultures, but in vivo only very few MFPCs were observed in obstructed kidneys, irrespective of BMP-6 genotype. The obstructed kidneys of BMP-6 null mice showed 2.2-fold more iron deposition, in association with 3.3-fold higher expression of the oxidative stress marker HO-1. Thus, ureteral obstruction leads to down-regulation of BMP-6 expression, and BMP-6 deficiency aggravates tubulointerstitial damage and fibrosis independent of BMP-7. This process appears to involve loss of both direct anti-inflammatory and antifibrotic action and indirect suppressive effects on renal iron deposition, oxidative stress, and MFPCs.
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