ArticleKidney international2018
CXCL12 blockade preferentially regenerates lost podocytes in cortical nephrons by targeting an intrinsic podocyte-progenitor feedback mechanism.
Article in Kidney international, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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
54 citing papers in PubMed, 98 citations in OpenAlex.
- Cell-cell crosstalk in kidney health and disease.Nature reviews. Nephrology · 2026Review
- Piezo1-Mediated Mechanotransduction: Orchestrating the Dynamic Response of Podocytes and Parietal Epithelial Cells to Mechanical Stress.Acta physiologica (Oxford, England) · 2026Review
- Slight acceleration in podocyte mRNA loss in preterm-born children aged 3-5 years.Pediatric nephrology (Berlin, Germany) · 2026Article
- Integrated Transcriptomic and Machine Learning Analyses Identify KCNN3 and TLR10 as Candidate Cell-Type-Associated Molecules in Idiopathic Membranous Nephropathy.International journal of general medicine · 2026Article
- Podocytopathies.Nature reviews. Disease primers · 2025Review
- Mechanisms and Therapeutic Perspectives of Podocyte Aging in Podocytopathies.International journal of molecular sciences · 2025Review
- The Life of a Kidney Podocyte.Acta physiologica (Oxford, England) · 2025Review
- Podocyte YAP and TAZ hyperactivation drives glomerular epithelial proliferative diseases in mice and humans.Science translational medicine · 2025Article
- Piezo1, F-Actin Remodeling, and Podocyte Survival and Regeneration.Journal of the American Society of Nephrology : JASN · 2025Article
- Safranal Ameliorates Renal Damage, Inflammation, and Podocyte Injury in Membranous Nephropathy via SIRT/NF-κB Signalling.Current medical science · 2025Article
- Article
- Dual blockade of DPP-4 and CXCL12/CXCR4 axes synergistically protects podocytes in lupus nephritis.Frontiers in pharmacology · 2025Article
- Histopathologic Analysis of Human Kidney Spatial Transcriptomics Data: Toward Precision Pathology.The American journal of pathology · 2025Article
- Transplantation of decellularized porcine kidney grafts repopulated with primary human cells demonstrates filtration function in pigs.Communications medicine · 2024Article
- Modeled microgravity unravels the roles of mechanical forces in renal progenitor cell physiology.Stem cell research & therapy · 2024Article
- Combination therapy with DHA and BMSCs suppressed podocyte injury and attenuated renal fibrosis by modulating the TGF-Renal failure · 2023Article
- Preparation of Human Kidney Progenitor Cultures and Their Differentiation into Podocytes.Bio-protocol · 2023Article
- Comparative evaluation of glomerular morphometric techniques reveals differential technical artifacts between focal segmental glomerulosclerosis and normal glomeruli.Physiological reports · 2023Article
- Inhibition of clonal expansion of parietal epithelial cells and crescent-podocyte transition in severe glomerulonephritis: on the way to targeted therapy?Clinical kidney journal · 2023Article
- Article
Corrections and comments
- Commented on by
- Commented on by
Authors and funding
16 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Insufficient podocyte regeneration after injury is a central pathomechanism of glomerulosclerosis and chronic kidney disease. Podocytes constitutively secrete the chemokine CXCL12, which is known to regulate homing and activation of stem cells; hence we hypothesized a similar effect of CXCL12 on podocyte progenitors. CXCL12 blockade increased podocyte numbers and attenuated proteinuria in mice with Adriamycin-induced nephropathy. Similar studies in lineage-tracing mice revealed enhanced de novo podocyte formation from parietal epithelial cells in the setting of CXCL12 blockade. Super-resolution microscopy documented full integration of these progenitor-derived podocytes into the glomerular filtration barrier, interdigitating with tertiary foot processes of neighboring podocytes. Quantitative 3D analysis revealed that conventional 2D analysis underestimated the numbers of progenitor-derived podocytes. The 3D analysis also demonstrated differences between juxtamedullary and cortical nephrons in both progenitor endowment and Adriamycin-induced podocyte loss, with more robust podocyte regeneration in cortical nephrons with CXCL12 blockade. Finally, we found that delayed CXCL12 inhibition still had protective effects. In vitro studies found that CXCL12 inhibition uncoupled Notch signaling in podocyte progenitors. These data suggest that CXCL12-driven podocyte-progenitor feedback maintains progenitor quiescence during homeostasis, but also limits their intrinsic capacity to regenerate lost podocytes, especially in cortical nephrons. CXCL12 inhibition could be an innovative therapeutic strategy in glomerular disorders.
Indexed as
Identifiers
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.