ArticleNature communications2025
Tracing the origin of myofibroblasts in kidney fibrosis.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Compensatory Mitophagy via NEDD4/HIF-1α/BNIP3 Pathway Restrains EndMT and Renal Allograft Interstitial Fibrosis Induced by TNFα.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Pharmacological targeting of kidney fibrosis: druggable mechanisms, translational models, and emerging antifibrotic therapies.Clinical kidney journal · 2026Review
- The Lactate-lactylation circuitry in kidney fibrosis: cellular crosstalk from tubular metabolic reprogramming to macrophage effector functions.Seminars in immunopathology · 2026Review
- Beyond EMT: Mesenchymal drift as an emerging driver of stromal-immune reprogramming in prostate cancer.iScience · 2026Review
- Review
- Knowledge Mapping of Macrophages in Renal Fibrosis: A Bibliometric Analysis from 2014 to 2025.Journal of inflammation research · 2026Review
- The Mechanism and Application of Traditional Chinese Medicine Nano-Formulations in the Treatment of Renal Fibrosis.International journal of nanomedicine · 2026Review
- Kidney angiopoietin-like protein 4 regulates fibrotic responses in diabetic kidney disease.Frontiers in pharmacology · 2026Review
- Single-Cell and Spatial Transcriptomics in Renal Injury and Fibrosis Research.Kidney diseases (Basel, Switzerland)Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Kidney fibrosis is a key pathological feature of chronic kidney disease (CKD), characterized by the activation and accumulation of αSMA-positive myofibroblasts. The cellular origin of myofibroblasts in kidney fibrosis has been a subject of extensive research and debate. Previous studies suggested that myofibroblasts might arise from various cellular sources through mesenchymal transition processes, including epithelial-mesenchymal transition (EMT) of tubular epithelial cells (TECs), endothelial-mesenchymal transition (EndoMT), and macrophage-mesenchymal transition (MMT) of bone marrow-derived cells. In this study, we systematically investigated the origin of myofibroblasts using renal cell lineage tracing tools during kidney fibrosis. Our findings indicated the absence of EMT, EndoMT, and MMT contributing to myofibroblasts, whereas resident fibroblasts were the primary source. Next, we developed and employed specialized dual recombinase-mediated lineage tracing tools, including EMTracer, EndoMTracer, and MMTracer, which revealed reversible partial mesenchymal transition occurring predominantly in the renal urothelial cells (UroCs) and parietal epithelial cells (PECs), minimally in endothelial cells, and not in TECs or macrophages. Our work elucidated the contribution of both complete and partial mesenchymal transition in various renal cell lineages and revealed the origin of myofibroblasts during kidney fibrosis, which may provide important insights into the diagnosis and treatment of CKD.
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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.