ArticleJournal of the American Society of Nephrology : JASN2021
Identification of an Altered Matrix Signature in Kidney Aging and Disease.
Article in Journal of the American Society of Nephrology : JASN, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.
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Who cites it
48 citing papers in PubMed, 1 synthesis or guideline pooled it, 74 citations in OpenAlex.
- Potential Renal Damage Biomarkers in Alport Syndrome-A Review of the Literature.International journal of molecular sciences · 2022Pooled it
- SMOC2 promotes partial epithelial-mesenchymal transition and maladaptive repair in renal tubular epithelial cells.JCI insight · 2026Article
- Ageing impacts extracellular matrix turnover and remodelling in the kidney.Matrix biology plus · 2026Article
- Accelerated basement membrane remodeling and serum matrix fragments as biomarkers of fibrosis in Alport syndrome.Cell reports · 2026Article
- Biochemical signals from the extracellular matrix in inflammation and tumour immunology.Nature reviews. Immunology · 2026Review
- Imaging-based organ-specific aging clock predicts human diseases and mortality.NPJ digital medicine · 2026Article
- Review
- Basement membranes at a glance.Journal of cell science · 2025Review
- A model of basement membrane-related regulators for prediction of prognoses in esophageal cancer and verification in vitro.BMC cancer · 2025Article
- Resistance physical exercise modulates metabolic adipokines, decreases body weight, and improves glomerular filtration in patients with chronic kidney disease in hemodialysis.Molecular and cellular biochemistry · 2025Article
- Collagen formation, function and role in kidney disease.Nature reviews. Nephrology · 2025Review
- Biomarkers for the early diagnosis of Alport syndrome and associated kidney damage.Childhood kidney diseases · 2025Review
- Multiomics Analysis Reveals Therapeutic Targets for Chronic Kidney Disease With Sarcopenia.Journal of cachexia, sarcopenia and muscle · 2025Article
- Evaluation of ovarian stiffness and its biological mechanism using shear wave elastography in polycystic ovary syndrome.Scientific reports · 2025Article
- IncreasedWellcome open research · 2025Article
- Mechanisms of assembly and remodelling of the extracellular matrix.Nature reviews. Molecular cell biology · 2024Review
- Pathological mechanisms of kidney disease in ageing.Nature reviews. Nephrology · 2024Review
- Identification and validation of basement membrane-associated gene AGRN as prognostic and immune-associated biomarkers in colorectal cancer patients.Journal of cellular and molecular medicine · 2024Article
- Comprehensive evaluation of genes related to basement membrane in hepatocellular carcinoma.Aging · 2024Article
- Role of biophysics and mechanobiology in podocyte physiology.Nature reviews. Nephrology · 2024Review
Corrections and comments
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Authors and funding
16 authors at 8 institutions in 2 countries.
Funding
Abstract
backgroundAccumulation of extracellular matrix in organs and tissues is a feature of both aging and disease. In the kidney, glomerulosclerosis and tubulointerstitial fibrosis accompany the decline in function, which current therapies cannot address, leading to organ failure. Although histologic and ultrastructural patterns of excess matrix form the basis of human disease classifications, a comprehensive molecular resolution of abnormal matrix is lacking.
methodsUsing mass spectrometry-based proteomics, we resolved matrix composition over age in mouse models of kidney disease. We compared the changes in mice with a global characterization of human kidneymatrix during aging and to existing kidney disease datasets to identify common molecular features.
resultsUltrastructural changes in basement membranes are associated with altered cell adhesion and metabolic processes and with distinct matrix proteomes during aging and kidney disease progression in mice. Within the altered matrix, basement membrane components (laminins, type IV collagen, type XVIII collagen) were reduced and interstitial matrix proteins (collagens I, III, VI, and XV; fibrinogens; and nephronectin) were increased, a pattern also seen in human kidney aging. Indeed, this signature of matrix proteins was consistently modulated across all age and disease comparisons, and the increase in interstitial matrix was also observed in human kidney disease datasets.
conclusionsThis study provides deep molecular resolution of matrix accumulation in kidney aging and disease, and identifies a common signature of proteins that provides insight into mechanisms of response to kidney injury and repair.
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