ReviewCurrent opinion in nephrology and hypertension2024
New tools to study renal fibrogenesis.
Review in Current opinion in nephrology and hypertension, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed.
- Exacerbation of renal interstitial fibrosis by the UHRF1/G9a axis through epigenetic silencing of KLF15.Renal failure · 2026Article
- Cell-cell crosstalk in kidney health and disease.Nature reviews. Nephrology · 2026Review
- Dissecting Normal and Abnormal Human Kidney Development Using Multiomics.Journal of the American Society of Nephrology : JASN · 2026Review
- Association Between Blood Lead Levels and Diabetic Kidney Disease: A Cross-sectional Analysis of NHANES Data (1999-2018).Current molecular medicine · 2026Article
- Protecting kidney function: from mechanisms to therapeutic targets and traditional Chinese medicine.Renal failure · 2025Review
- Spatial multi-omics: deciphering technological landscape of integration of multi-omics and its applications.Journal of hematology & oncology · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purpose of reviewKidney fibrosis is a key pathological aspect and outcome of chronic kidney disease (CKD). The advent of multiomic analyses using human kidney tissue, enabled by technological advances, marks a new chapter of discovery in fibrosis research of the kidney. This review highlights the rapid advancements of single-cell and spatial multiomic techniques that offer new avenues for exploring research questions related to human kidney fibrosis development. RECENT
findingsWe recently focused on understanding the origin and transition of myofibroblasts in kidney fibrosis using single-cell RNA sequencing (scRNA-seq) [1] . We analysed cells from healthy human kidneys and compared them to patient samples with CKD. We identified PDGFRα+/PDGFRβ+ mesenchymal cells as the primary cellular source of extracellular matrix (ECM) in human kidney fibrosis. We found several commonly shared cell states of fibroblasts and myofibroblasts and provided insights into molecular regulators. Novel single-cell and spatial multiomics tools are now available to shed light on cell lineages, the plasticity of kidney cells and cell-cell communication in fibrosis. SUMMARY: As further single-cell and spatial multiomic approaches are being developed, opportunities to apply these methods to human kidney tissues expand similarly. Careful design and optimisation of the multiomic experiments are needed to answer questions related to cell lineages, plasticity and cell-cell communication in kidney fibrosis.
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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.