ReviewJournal of the American Society of Nephrology : JASN2013
Regulatory T cells in AKI.
Review in Journal of the American Society of Nephrology : JASN, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02530359 (Pirfenidone Effect on the Recovery of Renal Function in Patients With Septic Acute Kidney Injury), which is not on this map. Cited by 58 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Pirfenidone Effect on the Recovery of Renal Function in Patients With Septic Acute Kidney Injury
Who cites it
58 citing papers in PubMed.
- Avidity-controlled biotherapeutic delivery systems for the treatment of ischemia-reperfusion acute kidney injury.bioRxiv : the preprint server for biology · 2026Article
- Abnormal lipid metabolism in senescent renal tubular cells in diabetic nephropathy.Cellular and molecular life sciences : CMLS · 2026Review
- A stage-based framework to interpret regulatory T cell biology after heart transplantation.Frontiers in cardiovascular medicine · 2026Review
- Adenosine receptors and acute kidney injury: perspectives for future therapy.Purinergic signalling · 2025Review
- The Role of Mitochondrial AKT1 Signaling in Renal Tubular Injury of Metabolic Syndrome.Kidney international reports · 2025Article
- Mechanisms Underlying the Impact of Interleukin Family on Acute Kidney Injury: Pathogenesis, Progression, and Therapy.Research (Washington, D.C.) · 2025Review
- Long Non-coding RNA NEAT1 , NOD-Like Receptor Family Protein 3 Inflammasome, and Acute Kidney Injury.Journal of the American Society of Nephrology : JASN · 2024Article
- From Acute to Chronic: Unraveling the Pathophysiological Mechanisms of the Progression from Acute Kidney Injury to Acute Kidney Disease to Chronic Kidney Disease.International journal of molecular sciences · 2024Review
- The role of regulatory T cells in the pathogenesis of acute kidney injury.Journal of cellular and molecular medicine · 2023Article
- Podoplanin: A potential therapeutic target for thrombotic diseases.Frontiers in neurology · 2023Review
- Th17/Regulatory T-Cell Imbalance and Acute Kidney Injury in Patients with Sepsis.Journal of clinical medicine · 2022Article
- Nutrition, Immunology, and Kidney: Looking Beyond the Horizons.Current nutrition reports · 2022Review
- Augmenter of liver regeneration protects the kidney against ischemia-reperfusion injury by inhibiting necroptosis.Bioengineered · 2022Article
- Repair phase modeling of ischemic acute kidney injury: recovery vs. transition to chronic kidney disease.American journal of translational research · 2022Article
- Inhibition of the IRE1/JNK pathway in renal tubular epithelial cells attenuates ferroptosis in acute kidney injury.Frontiers in pharmacology · 2022Article
- Tubular mitochondrial AKT1 is activated during ischemia reperfusion injury and has a critical role in predisposition to chronic kidney disease.Kidney international · 2021Article
- T helper 17 cells in the pathophysiology of acute and chronic kidney disease.Kidney research and clinical practice · 2021Article
- Review
- Association of Apoptosis-Mediated CD4Frontiers in cardiovascular medicine · 2021Article
- Mesenchymal Stem Cell Protects Injured Renal Tubular Epithelial Cells by Regulating mTOR-Mediated Th17/Treg Axis.Frontiers in immunology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Human AKI is manifested by inflammation, and an early feature in the pathogenesis is the accumulation of immune cells in the kidney. To understand the pathophysiology of AKI, results from animal models have shown a causal relation between the leukocyte activation and infiltration to the kidney after kidney ischemia-reperfusion. Blocking the activation or trafficking of proinflammatory leukocytes into the kidney preserves renal function and histologic integrity. In contrast, the anti-inflammatory lymphocytes called regulatory T cells have an intrinsic renal-protective function and may represent a novel therapeutic approach and/or target for pharmacological manipulation to ameliorate AKI. This review will highlight the recent insight gained into the role and mechanisms of regulatory T cells in AKI.
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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.