ArticleJournal of the American Society of Nephrology : JASN2013
Epithelial cell TGFβ signaling induces acute tubular injury and interstitial inflammation.
Article 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. Cited by 53 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
53 citing papers in PubMed, 75 citations in OpenAlex.
- Transforming growth factor-β in kidney disease in dogs and cats: a review of the evidence of its role in renal fibrosis.Journal of veterinary internal medicine · 2026Review
- Spatiotemporal Control of Intercellular Crosstalk: A New Therapeutic Paradigm for Halting Acute Kidney Injury to Chronic Kidney Disease Transition.Biomolecules · 2026Review
- Melatonin Administration Attenuates High-Fat-Diet-Induced Renal Damage in Wistar Rats.Biomolecules · 2025Article
- Inhibition of eCIRP attenuates PANoptosis and renal fibrosis.American journal of physiology. Renal physiology · 2025Article
- Early single session of hyperbaric oxygen therapy mitigates renal apoptosis in lipopolysaccharides-induced endotoxemia in rats.Kidney research and clinical practice · 2025Article
- Article
- Repair of Isoaspartyl Residues by PCMT1 and Kidney Fibrosis.Journal of the American Society of Nephrology : JASN · 2025Article
- Urinary RANTES and MCP-1 as noninvasive biomarkers for differential diagnosis and prediction of treatment response in acute interstitial nephritis.Clinical kidney journal · 2025Article
- Modulation of TGF-β signaling new approaches toward kidney disease and fibrosis therapy.International journal of biological sciences · 2025Review
- The effectiveness of antioxidant agents in delaying progression of diabetic nephropathy: A systematic review of randomized controlled trials.BioImpacts : BI · 2025Review
- Mutational burden of XPNPEP3 leads to defects in mitochondrial complex I and cilia in NPHPL1.iScience · 2023Article
- Nicorandil protects podocytes via modulation of antioxidative capacity in acute puromycin aminonucleoside-induced nephrosis in rats.American journal of physiology. Renal physiology · 2023Article
- Renal function protection and the mechanism of ginsenosides: Current progress and future perspectives.Frontiers in pharmacology · 2023Review
- The role of the SGK3/TOPK signaling pathway in the transition from acute kidney injury to chronic kidney disease.Frontiers in pharmacology · 2023Article
- Review
- Inactivation of fatty acid amide hydrolase protects against ischemic reperfusion injury-induced renal fibrogenesis.Biochimica et biophysica acta. Molecular basis of disease · 2022Article
- Renal biomarkers in cats: A review of the current status in chronic kidney disease.Journal of veterinary internal medicine · 2022Review
- SARS-CoV-2 N Protein Induces Acute Kidney Injury via Smad3-Dependent G1 Cell Cycle Arrest Mechanism.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Interaction Between Intrinsic Renal Cells and Immune Cells in the Progression of Acute Kidney Injury.Frontiers in medicine · 2022Review
- Estradiol Ameliorates Acute Kidney Ischemia-Reperfusion Injury by Inhibiting the TGF-βRI-SMAD Pathway.Frontiers in immunology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
TGFβ signaling plays a central role in the development of acute and chronic kidney diseases. Previous in vivo studies involved systemic alteration of TGFβ signaling, however, limiting conclusions about the direct role of TGFβ in tubular cell injury. Here, we generated a double transgenic mouse that inducibly expresses a ligand-independent constitutively active TGFβ receptor type 1 (TβR1) kinase specifically in tubular epithelial cells, with expression restricted by the Pax8 promoter. In this model, activation of TGFβ signaling in the tubular epithelium alone was sufficient to cause AKI characterized by marked tubular cell apoptosis and necrosis, oxidative stress, dedifferentiation and regenerative cell proliferation, reduced renal function, and interstitial accumulation of inflammatory cells. This tubular injury was associated with mitochondrial-derived generation of reactive oxygen species (ROS), but cell damage and apoptosis were partially independent of mitochondrial-derived ROS. TβR1 signaling-induced tubular injury also associated with significant leukocyte infiltration consisting of F4/80(+) macrophages, CD11c(+) F4/80(+) dendritic cells, CD11c(+) F4/80(-) Ly6C(high) dendritic cells/monocytes, and T cells. Inhibition of mitochondrial-derived ROS significantly reduced accumulation of CD11c(+) F4/80(+) dendritic cells and T cells, suggesting a role for ROS in the activation and recruitment of the adaptive immune response to tubular injury. Taken together, these results suggest that TGFβ signaling in the tubular epithelium alone is sufficient to cause acute tubular injury and inflammation; therefore, TGFβ may be a mechanistic link between acute injury and chronic progression of kidney disease.
Indexed as
Identifiers
What OpenQuestion holds
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.