ArticleBiochemistry and biophysics reports2025
Single-cell spatial transcriptomics reveals pathogenic mechanism of renal fibrosis in imiquimod-induced lupus nephritis in mice.
Article in Biochemistry and biophysics reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.
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Who cites it
5 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Enhancing RNA Capture Efficiency in Spatial Transcriptomics: A Review of Innovative Technologies and Strategies.International journal of molecular sciences · 2025Pooled it
- Engineering autoimmune disease models using organoids: Harnessing microenvironmental engineering for precision medicine and immunological recapitulation.Bioengineering & translational medicine · 2026Review
- Macrophage Plasticity and Regulatory Networks During the Transition from Inflammation to Fibrosis in the Kidney.Life (Basel, Switzerland) · 2025Review
- Mitochondrial immunometabolism in sepsis: orchestrating macrophage polarization and dysfunction.European journal of medical research · 2025Review
- Spatial transcriptomic landscape and cellular neighborhood heterogeneity in cervical cancer: integrative single-cell and spatial RNA sequencing analysis.Discover oncology · 2025Article
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Authors and funding
8 authors.
Funding
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Abstract
A deeper understanding of the cellular and molecular pathology pathways of renal fibrosis in lupus nephritis (LN) is essential for the accurate disease assessment and the development of novel therapeutic strategies. In this study, we employed advanced spatial transcriptomics technique to elucidate the underlying mechanism of renal fibrosis in mouse kidneys. By establishing single-nuclei and spatial transcriptomic maps for LN and control kidneys, we identified a significant activation and proliferation of fibroblasts predominantly in the inner stripe of outer medulla (ISOM) region and pinpointed a set of specific gene signatures associated with fibrosis. Furthermore, we discovered a class of pro-fibrotic macrophage subtype, Lyz2 macrophage, that promotes myofibroblast activation. We elucidated the intricate molecular interplay mechanisms involved in this process. Our study also delved into the glomerular region, revealed disease-induced alterations in gene expression and identified potential novel therapeutic targets.
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