ReviewJournal of the American Society of Nephrology : JASN2013
Integrins in kidney disease.
Review in Journal of the American Society of Nephrology : JASN, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
72 citing papers in PubMed, 1 synthesis or guideline pooled it, 124 citations in OpenAlex.
- Genetic and environmental factors associated with alteration of filtration slit proteins and their functions: a scoping review.Frontiers in nephrology · 2025Pooled it
- Potential Role of the Urokinase-Type Plasminogen Activator Receptor-Integrin β3 Axis in Podocyte Adhesion Instability and Loss.Kidney international reports · 2026Article
- Ultrasound-guided renal artery administration of angiopoietin-1 RNA therapy slows the progression of preclinical WT1 glomerular disease.Science translational medicine · 2026Article
- Functional characterization of podocyte-expressed THSD7A in experimental membranous nephropathy.JCI insight · 2026Article
- Applying dendrimer nanoprobes to the diagnosis and evaluation of kidney fibrosis.Nanomedicine (London, England) · 2026Review
- Matricellular protein SMOC2 safeguards tubular integrity in acute kidney injury via integrin β3-dependent inhibition of CCND1-CDK4/6 axis.Molecular biomedicine · 2026Article
- Integrins in the kidney - beyond the matrix.Nature reviews. Nephrology · 2025Review
- Case Report: Severe kidney involvement in a case of very early onset inflammatory bowel disease.Frontiers in immunology · 2025Article
- Integrin αM promotes macrophage alternative M2 polarization in hyperuricemia-related chronic kidney disease.MedComm · 2024Article
- Minimal Change Disease: Pathogenetic Insights from Glomerular Proteomics.International journal of molecular sciences · 2024Article
- Characterization of glomerular basement membrane components within pediatric glomerular diseases.Clinical kidney journal · 2024Article
- Assessing Kidney Injury Induced by Mercuric Chloride in Guinea Pigs with In Vivo and In Vitro Experiments.International journal of molecular sciences · 2023Article
- Reduced methylation correlates with diabetic nephropathy risk in type 1 diabetes.The Journal of clinical investigation · 2023Article
- The Mechanism of Hyperglycemia-Induced Renal Cell Injury in Diabetic Nephropathy Disease: An Update.Life (Basel, Switzerland) · 2023Review
- Cell-Matrix Interactions in Renal Fibrosis.Kidney and dialysis · 2022Article
- Integrin α3 negative podocytes: A gene expression study.Matrix biology plus · 2022Article
- Plasma proteomic characterization of the development of acute kidney injury in early sepsis patients.Scientific reports · 2022Article
- Anti-ANGPTL3-FLD monoclonal antibody treatment ameliorates podocyte lesions through attenuating mitochondrial damage.Cell death & disease · 2022Article
- The Perspective of Vitamin D on suPAR-Related AKI in COVID-19.International journal of molecular sciences · 2022Review
- Integrin β1/Cell Surface GRP78 Complex Regulates TGFβ1 and Its Profibrotic Effects in Response to High Glucose.Biomedicines · 2022Article
12 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 2 countries.
Funding
Abstract
A major hallmark of chronic kidney injury is fibrosis, which is characterized by increased accumulation of extracellular matrix components that replace the damaged tissue. Normally, the synthesis and degradation of extracellular matrix components are finely regulated; however, when matrix replacement goes unchecked, there is unwanted and irreversible tissue scarring with consequent organ damage, organ failure, and, in certain cases, death. Many factors, including cell-matrix interactions, play a role in the development of renal fibrosis. Cell-matrix interactions are made possible by integrins, a family of transmembrane receptors that, upon binding to the extracellular matrix, activate intracellular signaling. Thus, they control various cell functions, including survival, proliferation, migration, and matrix homeostasis. Genetic mutations in humans and the development of animal models lacking integrins in selective parts of the kidney have improved our understanding of molecular mechanisms and pathways controlling matrix remodeling in kidney disease. Here we outline the major integrins involved in kidney disease and some of the major molecular mechanisms whereby integrins contribute to kidney fibrosis.
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What OpenQuestion holds
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.