ArticleThe Journal of clinical investigation2020
Methylation in pericytes after acute injury promotes chronic kidney disease.
Article in The Journal of clinical investigation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 79 citations in OpenAlex.
- Transition from acute kidney injury to chronic kidney disease: molecular mechanisms and therapeutic interventions.Molecular biomedicine · 2026Review
- From Single-Cell Clusters to Causality: ITCH Engagement for CKD Uncovered by Integrative Analysis of MR and MAGMA.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Profibrotic macrophage-derived CXCL4 promotes pericyte-to-myofibroblast transition after spinal cord injury.Journal of orthopaedic translation · 2026Article
- Protecting kidney function: from mechanisms to therapeutic targets and traditional Chinese medicine.Renal failure · 2025Review
- Role of microvascular pericyte dysfunction in antibody-mediated rejection following kidney transplantation.Renal failure · 2025Article
- Pericytes in tissue fibrosis.American journal of physiology. Cell physiology · 2025Review
- Gavage versus dietary adenine administration is more effective for the female mouse model of chronic kidney disease.Scientific reports · 2025Article
- Pericytes and Diabetic Microangiopathies: Tissue Resident Mesenchymal Stem Cells with High Plasticity and Regenerative Capacity.International journal of molecular sciences · 2025Review
- Integration of DNA Methylome and Transcriptome Analysis to Identify Novel Epigenetic Targets in the Acute Kidney Injury-Chronic Kidney Disease Transition.Biomolecules · 2025Article
- Molecular mechanisms and therapeutic interventions in acute kidney injury: a literature review.BMC nephrology · 2025Review
- Hypermethylation and suppression of microRNA219a-2 activates the ALDH1L2/GSH/PAI-1 pathway for fibronectin degradation in renal fibrosis.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Adenine-induced animal model of chronic kidney disease: current applications and future perspectives.Renal failure · 2024Review
- FUT8 upregulates CD36 and its core fucosylation to accelerate pericyte-myofibroblast transition through the mitochondrial-dependent apoptosis pathway during AKI-CKD.Molecular medicine (Cambridge, Mass.) · 2024Article
- Epigenetic reprogramming driving successful and failed repair in acute kidney injury.Science advances · 2024Article
- Crosstalk among proximal tubular cells, macrophages, and fibroblasts in acute kidney injury: single-cell profiling from the perspective of ferroptosis.Human cell · 2024Article
- DNA methylation in peripheral blood is associated with renal aging and renal function decline: a national community study.Clinical epigenetics · 2024Article
- Article
- Hypoxic Inducible Factor Stabilization in Pericytes beyond Erythropoietin Production: The Good and the Bad.Antioxidants (Basel, Switzerland) · 2024Review
- Nucleic acid and protein methylation modification in renal diseases.Acta pharmacologica Sinica · 2024Review
- Pyruvate kinase M2 regulates kidney fibrosis through pericyte glycolysis during the progression from acute kidney injury to chronic kidney disease.Cell proliferation · 2024Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The origin and fate of renal myofibroblasts is not clear after acute kidney injury (AKI). Here, we demonstrate that myofibroblasts were activated from quiescent pericytes (qPericytes) and the cell numbers increased after ischemia/reperfusion injury-induced AKI (IRI-AKI). Myofibroblasts underwent apoptosis during renal recovery but one-fifth of them survived in the recovered kidneys on day 28 after IRI-AKI and their cell numbers increased again after day 56. Microarray data showed the distinctive gene expression patterns of qPericytes, activated pericytes (aPericytes, myofibroblasts), and inactivated pericytes (iPericytes) isolated from kidneys before, on day 7, and on day 28 after IRI-AKI. Hypermethylation of the Acta2 repressor Ybx2 during IRI-AKI resulted in epigenetic modification of iPericytes to promote the transition to chronic kidney disease (CKD) and aggravated fibrogenesis induced by a second AKI induced by adenine. Mechanistically, transforming growth factor-β1 decreased the binding of YBX2 to the promoter of Acta2 and induced Ybx2 hypermethylation, thereby increasing α-smooth muscle actin expression in aPericytes. Demethylation by 5-azacytidine recovered the microvascular stabilizing function of aPericytes, reversed the profibrotic property of iPericytes, prevented AKI-CKD transition, and attenuated fibrogenesis induced by a second adenine-AKI. In conclusion, intervention to erase hypermethylation of pericytes after AKI provides a strategy to stop the transition to CKD.
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