ArticleAmerican journal of physiology. Renal physiology2013
Macrophage-specific deletion of transforming growth factor-β1 does not prevent renal fibrosis after severe ischemia-reperfusion or obstructive injury.
Article in American journal of physiology. Renal physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 72 citations in OpenAlex.
- Immune microenvironment in autosomal dominant polycystic kidney disease.Genes & diseases · 2026Review
- Precision nanotherapeutics for kidney disease: targeting inflammation and maladaptive repair.International urology and nephrology · 2026Review
- XBP1s-Orchestrated Soluble Mediators: Participants of Oxidative Stress in Renal Ischemia-Reperfusion Injury Following Donation After Circulatory Death.Mediators of inflammation · 2026Review
- Innate immune cells in acute and chronic kidney disease.Nature reviews. Nephrology · 2025Review
- USP25 stabilizes STAT6 to promote IL-4-induced macrophage M2 polarization and fibrosis.International journal of biological sciences · 2025Article
- Efferocytosis in Homeostasis.Advances in experimental medicine and biology · 2025Review
- Neu1 deficiency and fibrotic lymph node microenvironment lead to imbalance in M1/M2 macrophage polarization.Frontiers in immunology · 2024Article
- A comparative study on the effects of biodegradable high-purity magnesium screw and polymer screw for fixation in epiphyseal trabecular bone.Regenerative biomaterials · 2024Article
- The Role of Immune Cells in the Pathogenesis of Idiopathic Pulmonary Fibrosis.Medicina (Kaunas, Lithuania) · 2023Review
- XBP1 Modulates the Aging Cardiorenal System by Regulating Oxidative Stress.Antioxidants (Basel, Switzerland) · 2023Review
- HCK induces macrophage activation to promote renal inflammation and fibrosis via suppression of autophagy.Nature communications · 2023Article
- Macrophages and fibrosis: how resident and infiltrating mononuclear phagocytes account for organ injury, regeneration or atrophy.Frontiers in immunology · 2023Review
- TGF-β1 peptide-based inhibitor P144 ameliorates renal fibrosis after ischemia-reperfusion injury by modulating alternatively activated macrophages.Cell proliferation · 2022Article
- Immune-mediated tubule atrophy promotes acute kidney injury to chronic kidney disease transition.Nature communications · 2022Article
- Conditional deletion of myeloid-specific mitofusin 2 but not mitofusin 1 promotes kidney fibrosis.Kidney international · 2022Article
- The antimicrobial peptide YD attenuates inflammationActa pharmaceutica Sinica. B · 2021Article
- The Role of Macrophages in Kidney Fibrosis.Frontiers in physiology · 2021Review
- Article
- Transforming growth factor-β in tissue fibrosis.The Journal of experimental medicine · 2020Review
- Article
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3 authors at 1 institution in 1 country.
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Abstract
Macrophage infiltration is a prominent feature of the innate immune response to kidney injury. The persistence of macrophages is associated with tubulointerstitial fibrosis and progression of chronic kidney disease. Macrophages are known to be major producers of transforming growth factor-β1 (TGF-β1), especially in the setting of phagocytosis of apoptotic cells. TGF-β1 has long been implicated as a central mediator of tissue scarring and fibrosis in many organ disease models, including kidney disease. In this study, we show that homozygous deletion of Tgfb1 in myeloid lineage cells in mice heterozygous for Tgfb1 significantly reduces kidney Tgfb1 mRNA expression and Smad activation at late time points after renal ischemia-reperfusion injury. However, this reduction in kidney Tgfb1 expression and signaling results in only a modest reduction of isolated fibrosis markers and does not lead to decreased interstitial fibrosis in either ischemic or obstructive injury models. Thus, targeting macrophage-derived TGF-β1 does not appear to be an effective therapy for attenuating progressive renal fibrosis after kidney injury.
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