ReviewNature reviews. Nephrology2025
Innate immune cells in acute and chronic kidney disease.
Review in Nature reviews. Nephrology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
33 citing papers in PubMed.
- Surfactant protein A (SP-A) alleviates acute kidney injury by reducing macrophage recruitment and M1 polarization.Journal of molecular histology · 2026Article
- Mechanisms of regeneration and maladaptive repair in acute kidney injury.Nature reviews. Nephrology · 2026Review
- [Protective effects and underlying mechanisms of bone marrow mesenchymal stem cells-derived apoptotic extracellular vesicles in acute kidney injury].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2026Article
- STK40 inhibits profibrotic Arg1Acta pharmacologica Sinica · 2026Article
- ELF3 links kidney function GWAS loci to maladaptive epithelial inflammation.Science advances · 2026Article
- Degradation reshapes the toxic identity of polylactic acid microplastics through MSR1-dependent immune decoding in mouse kidney.Particle and fibre toxicology · 2026Article
- iMSC-secreted factors preserve renal capillary networks and ameliorate fibrosis by interrupting the macrophage STING/CD8Stem cell research & therapy · 2026Article
- Article
- Stem cell therapies to modulate harmful immune responses in kidney disease: progress toward clinical validation.Stem cells (Dayton, Ohio) · 2026Review
- Ultrasound-activated piezoelectric Bi@Bi-MOF enables STING-mediated immunotherapy for implant-associated infections.Journal of nanobiotechnology · 2026Article
- Maternal obesity induces macrophage to myofibroblast transition in kidneys of male offspring through a pathway driven by 20-hydroxyeicosatetraenoic acid.Nature communications · 2026Article
- Nephrotoxicity of Immune Checkpoint Inhibitors in Mice with a Human Immune System.bioRxiv : the preprint server for biology · 2026Article
- Transition from acute kidney injury to chronic kidney disease: molecular mechanisms and therapeutic interventions.Molecular biomedicine · 2026Review
- The Aging Kidney and Acute Kidney Injury.Journal of the American Society of Nephrology : JASN · 2026Review
- Pharmaceutical Treatments for Typical CKD Comorbidities.Biomedicines · 2026Article
- Molecular mechanisms of acute inflammation: systemic responses and kidney-specific pathophysiology.Function (Oxford, England) · 2026Review
- Mitophagy and Cellular Homeostasis in Kidney Diseases: Mechanisms and Potential Therapeutics.International journal of biological sciences · 2026Review
- From immune dysregulation to renal injury: mechanistic insights and translational opportunities in immune-mediated nephropathies.Frontiers in cell and developmental biology · 2026Review
- Extracellular vesicles mediate immune regulation in acute kidney injury.Frontiers in immunology · 2026Review
- Total Glucosides of Paeony Alleviates Acute Kidney Injury by Inhibiting Dendritic Cells and T-Cell Communication.Advances in pharmacological and pharmaceutical sciences · 2026Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute kidney injury (AKI) and chronic kidney disease (CKD) are inter-related clinical and pathophysiological disorders. Cells of the innate immune system, such as granulocytes and macrophages, can induce AKI through the secretion of pro-inflammatory mediators such as cytokines, chemokines and enzymes, and the release of extracellular traps. In addition, macrophages and dendritic cells can drive the progression of CKD through a wide range of pro-inflammatory and pro-fibrotic mechanisms, and by regulation of the adaptive immune response. However, innate immune cells can also promote kidney repair after acute injury. These actions highlight the multifaceted nature of the way by which innate immune cells respond to signals within the kidney microenvironment, including interaction with the complement and coagulation cascades, cells of the adaptive immune system, intrinsic renal cells and infiltrating mesenchymal cells. The factors and mechanisms that underpin the ability of innate immune cells to contribute to renal injury or repair and to drive the progression of CKD are of great interest for understanding disease processes and for developing new therapeutic approaches to limit AKI and the AKI-to-CKD transition.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.