ArticleInternational journal of biological sciences2024
CD8 T cells induce the peritubular capillary rarefaction during AKI to CKD transition.
Article in International journal of biological sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed.
- Potential targets and molecular mechanisms of D-pinitol against acute kidney injury based on network pharmacology and experimental validation.Renal failure · 2026Article
- T-Cell Remodeling in Renal Fibrosis: From Acute Injury to Chronic Kidney Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Programmed cell death in kidney disease: integrated crosstalk among ferroptosis, pyroptosis, apoptosis, and cuproptosis.Apoptosis : an international journal on programmed cell death · 2026Review
- Gut microbiota and renal fibrosis: novel mechanistic insights and therapeutic potential.Acta pharmacologica Sinica · 2026Review
- T Cell-Independent Role of PD-L1 in Kidney Repair: Mitigation of Tubular DNA Damage via PD-L1/BRCA1 Interaction Following AKI.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Single-cell RNA sequencing and spatial transcriptomics in the discovery of kidney disease potential biomarkers: a narrative review.BMC nephrology · 2026Review
- Bio-hybrid nanovesicles with multimodal antioxidant and immunomodulatory functions attenuate acute kidney injury.Journal of nanobiotechnology · 2026Article
- iMSC-secreted factors preserve renal capillary networks and ameliorate fibrosis by interrupting the macrophage STING/CD8Stem cell research & therapy · 2026Article
- Stress-Dependent NF-κB Signaling in Acute Kidney Injury: Linking Inflammation, Autophagy, and Apoptosis.International journal of molecular sciences · 2026Review
- Transition from acute kidney injury to chronic kidney disease: molecular mechanisms and therapeutic interventions.Molecular biomedicine · 2026Review
- Refinement of renal T lymphocytes enrichment strategies: advancing the in-depth study of renal immune responses.Scientific reports · 2026Article
- Targeting GPR34 in damage-associated macrophages enhances anti-tumor immunity and the efficacy of Surufatinib in pancreatic cancer.Signal transduction and targeted therapy · 2026Article
- Vascular transcriptional and metabolic changes precede progressive intrarenal microvascular rarefaction in autosomal dominant polycystic kidney disease.American journal of physiology. Renal physiology · 2026Article
- Targeted inhibition of RGS19 alleviates renal fibrosis by restoring autophagy and modulating immune cell infiltration.Journal of nanobiotechnology · 2026Article
- Identification of Ferroptosis-Related Hub Genes and Immune Infiltration Landscape in Chronic Kidney Disease via Bioinformatics and Experimental Verification.Immunity, inflammation and disease · 2026Article
- Mechanistic Insights and Therapeutic Advances of Anti-Inflammatory Biologics in Immune-Mediated Glomerulonephritis: A Narrative Review.Journal of inflammation research · 2026Review
- Chronic Rejection in Facial Vascularized Composite Allotransplantation (fVCA).Results and problems in cell differentiation · 2026Review
- Adaptive immune cells and kidney function in older adults: sex-specific associations in the health and retirement study (HRS).Frontiers in aging · 2026Article
- Crosstalk between macrophages and adjacent cells in AKI to CKD transition.Renal failure · 2025Review
- Histone modification-mediated epigenetic regulation in AKI-to-CKD transition: a cell-type-specific perspective.Journal of translational medicine · 2025Review
Corrections and comments
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Authors and funding
13 authors.
Funding
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Abstract
Acute kidney injury (AKI) transformed to chronic kidney disease (CKD) is a critical clinical issue characterized by tubulointerstitial inflammation (TII) and fibrosis. However, the exact mechanism remains largely unclear. In this study, we used single-cell RNA sequencing (scRNA-seq) to obtain a high-resolution profile of T cells in AKI to CKD transition with a mice model of unilateral ischemia-reperfusion injury (uIRI). We found that T cells accumulated increasingly with the progression of AKI to CKD, which was categorized into 9 clusters. A notably increased proportion of CD8 T cells via self-proliferation occurred in the early stage of AKI was identified. Further study revealed that the CD8 T cells were recruited through CXCL16-CXCR6 pathway mediated by macrophages. Notably, CD8 T cells induced endothelial cell apoptosis via Fas ligand-Fas signaling. Consistently, increased CD8 T cell infiltration accompanied with peritubular capillaries (PTCs) rarefaction was observed in uIRI mice. More impressively, the loss of PTCs and renal fibrosis was remarkably ameliorated after the elimination of CD8 T cells. In summary, our study provides a novel insight into the role of CD8 T cells in the transition from AKI to CKD via induction of PTCs rarefaction, which could suggest a promising therapeutic target for AKI.
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