ArticleBritish journal of pharmacology2023
Jumonji domain-containing protein-3 (JMJD3) promotes myeloid fibroblast activation and macrophage polarization in kidney fibrosis.
Article in British journal of pharmacology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 47 citations in OpenAlex.
- KLF transcription factors in metabolic kidney disease: from podocyte protection to tubulointerstitial fibrosis.International urology and nephrology · 2026Review
- OLFM4 mediating ischemia/reperfusion-induced kidney injury by regulating renal tubular epithelial cells ferroptosis via GPX4.Molecular biology reports · 2026Article
- Macrophage RNA polymerase II subunit 5-mediating protein deficiency exacerbates kidney inflammation and fibrosis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- The role of interleukin-4 in acute kidney injury and chronic kidney disease: a literature review.BMC nephrology · 2026Review
- 15- Deoxy-Δ12,14-prostaglandin J2 upregulates COX-2 expression and PGEFrontiers in pharmacology · 2026Article
- Targeting DPP9 attenuates podocyte injury by regulating NRF2 antioxidant signaling.Frontiers in pharmacology · 2026Article
- Cell-state- and compartment-dependent PI3K/Akt redox signaling in chronic kidney disease: mechanisms and translational implications.Frontiers in pharmacology · 2026Review
- Critical role of transcription factor SOX4 in tubular epithelial cell dedifferentiation and fibroblast activation during kidney fibrosis.Kidney international · 2026Article
- Macrophage Plasticity and Regulatory Networks During the Transition from Inflammation to Fibrosis in the Kidney.Life (Basel, Switzerland) · 2025Review
- The Histone Demethylase Inhibitor GSK-J4 Attenuates Periodontal Bone Loss and Inflammation in a Rat Model of Periodontitis.Current medical science · 2025Article
- The multifaceted role of macrophages in kidney physiology and diseases.Frontiers in immunology · 2025Review
- A crucial role of miR-155 in the pathomechanism of acute kidney injury.Frontiers in pharmacology · 2025Review
- Homotherapy for heteropathy of chronic kidney disease and oligoasthenozoospermia through regulating SIRT1/NF-κB pathway by Shenqi pills.Frontiers in pharmacology · 2025Article
- Renoprotective effects of GHRH agonist MR409 is associated with reduced oxidative stress and ferroptosis in diabetic mice.Frontiers in pharmacology · 2025Article
- Enzymatic post-translational modifications of proteins in chronic kidney disease: mechanisms, regulation, and clinical significance.Frontiers in pharmacology · 2025Review
- Epigenetic regulation of transcription factors involved in NLRP3 inflammasome and NF-kB signaling pathways.Frontiers in immunology · 2025Review
- Macrophages: emerging targets for ulcerative colitis.Frontiers in immunology · 2025Review
- TEAD1 Prevents Necroptosis and Inflammation in Cisplatin-Induced Acute Kidney Injury Through Maintaining Mitochondrial Function.International journal of biological sciences · 2025Article
- Histone methylation modification and diabetic kidney disease: Potential molecular mechanisms and therapeutic approaches (Review).International journal of molecular medicine · 2024Review
- Advance on Chinese Medicine for Hypertensive Renal Damage: Focus on the Complex Molecular Mechanisms.Chinese journal of integrative medicine · 2024Review
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
background and purposeRenal fibrosis is a common feature of chronic kidney disease. Myeloid fibroblasts and macrophages contribute significantly to the pathogenesis of renal fibrosis. However, the molecular mechanisms underlying myeloid fibroblast activation and macrophage polarization are not fully understood. In this study, we examined the role of Jumonji domain-containing protein-3 (JMJD3) in myeloid fibroblast activation, macrophage polarization, and renal fibrosis development in a preclinical model of obstructive nephropathy. EXPERIMENTAL APPROACH: To examine the role of JMJD3 in renal fibrosis, we generated mice with global or myeloid cell-specific deletion of JMJD3, and we treated wild-type mice with vehicle or GSK-J4 (selective JMJD3 inhibitor). Mice were subjected to unilateral ureteral obstructive injury to induce renal fibrosis. KEY
resultsJMJD3 expression was significantly increased in the kidneys during the development of renal fibrosis, which was associated with an increase in H3K27 dimethylation. Mice with either global or myeloid JMJD3 deficiency exhibited significantly reduced total collagen deposition and extracellular matrix protein production, myeloid fibroblast activation and M2 macrophage polarization in the obstructed kidney. Moreover, IFN regulatory factor 4, a mediator of M2 macrophage polarization, was significantly induced in the obstructed kidneys, which was abolished by JMJD3 deficiency. Furthermore, pharmacological inhibition of JMJD3 with GSK-J4 attenuated kidney fibrosis, reduced myeloid fibroblast activation and suppressed M2 macrophage polarization in the obstructed kidney. CONCLUSION AND IMPLICATIONS: Our study identifies JMJD3 as a critical regulator of myeloid fibroblast activation, macrophage polarization, and renal fibrosis development. Therefore, JMJD3 may represent a promising therapeutic target for chronic kidney disease.
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