ArticleHypertension (Dallas, Tex. : 1979)2014
NFAT5 is protective against ischemic acute kidney injury.
Article in Hypertension (Dallas, Tex. : 1979), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 28 citations in OpenAlex.
- BPGM shapes NFAT5-driven cellular responses.Cellular and molecular life sciences : CMLS · 2026Article
- siRNA-mediated inhibition of NTT-MMP-2 reduces oxidative stress and apoptotic signaling in an ex vivo model of ischemia/reperfusion injury.Scientific reports · 2025Article
- Long Non-coding RNA MIR22HG Alleviates Ischemic Acute Kidney Injury by Targeting the miR-134-5p/NFAT5 axis.Inflammation · 2025Article
- TNF inhibits NKCC2 phosphorylation by a calcineurin-dependent pathway.American journal of physiology. Renal physiology · 2025Article
- Segment specific loss of NFAT5 function in the kidneys is sufficient to induce a global kidney injury like phenotype.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- NFAT5: a stress-related transcription factor with multiple functions in health and disease.Cell stress · 2025Review
- Serum amyloid A expression in liver promotes synovial macrophage activation and chronic arthritis via NFAT5.The Journal of clinical investigation · 2024Article
- Predicting proximal tubule failed repair drivers through regularized regression analysis of single cell multiomic sequencing.Nature communications · 2024Article
- TNF inhibits AQP2 expression via a miR137-dependent pathway.American journal of physiology. Renal physiology · 2024Article
- MicroRNA-195a-5p Regulates Blood Pressure by Inhibiting NKCC2A.Hypertension (Dallas, Tex. : 1979) · 2023Article
- The nuclear factor of activated T cells 5 (NFAT5) contributes to the renal corticomedullary differences in gene expression.Scientific reports · 2022Article
- Assessment of Physiological Rat Kidney Ageing-Implications for the Evaluation of Allograft Quality Prior to Renal Transplantation.Metabolites · 2022Article
- Single-nuclear transcriptomics reveals diversity of proximal tubule cell states in a dynamic response to acute kidney injury.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- LINC00963 targeting miR-128-3p promotes acute kidney injury process by activating JAK2/STAT1 pathway.Journal of cellular and molecular medicine · 2020Article
- Regulation of NKCC2B by TNF-α in response to salt restriction.American journal of physiology. Renal physiology · 2020Article
- Potential Role of Gene Regulator NFAT5 in the Pathogenesis of Diabetes Mellitus.Journal of diabetes research · 2020Review
- NFAT5 and HIF-1α Coordinate to Regulate NKCC1 Expression in Hippocampal Neurons After Hypoxia-Ischemia.Frontiers in cell and developmental biology · 2019Article
- Renal-Specific Silencing of TNF (Tumor Necrosis Factor) Unmasks Salt-Dependent Increases in Blood Pressure via an NKCC2A (NaHypertension (Dallas, Tex. : 1979) · 2018Article
- Upregulation of DARS2 by HBV promotes hepatocarcinogenesis through the miR-30e-5p/MAPK/NFAT5 pathway.Journal of experimental & clinical cancer research : CR · 2017Article
- Genistein Ameliorates Ischemia/Reperfusion-Induced Renal Injury in a SIRT1-Dependent Manner.Nutrients · 2017Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
NFAT5 is a transcription factor that protects the kidney from hypertonic stress and also is activated by hypoxia. We hypothesized that NFAT5 mitigates the extent of renal damage induced by ischemia-reperfusion injury (IRI). Mice were subjected to IRI by unilateral clamping of the left renal pedicle for 30 minutes followed by reperfusion. After 3 hours of reperfusion, the level of NFAT5 mRNA was similar in contralateral and clamped kidneys. However, after 48 hours, NFAT5 mRNA accumulation increased ≈3-fold in both outer medulla and medullary thick ascending limb tubules. NFAT1 levels were elevated at 3 hours but did not increase further at 48 hours. Mice were then either pretreated for 72 hours with an intrarenal injection of a lentivirus short-hairpin RNA construct to silence NFAT5 (enhanced green fluorescent protein-U6-N5-ex8) or a control vector (enhanced green fluorescent protein-U6) before induction of IRI. Neutrophil gelatinase-associated lipocalin and kidney ischemia molecule-1 mRNA levels increased after IRI and further increased after knockdown of NFAT5, suggesting that silencing of NFAT5 exacerbates renal damage during IRI. In contrast, silencing of NFAT1 had no effect on the levels of neutrophil gelatinase-associated lipocalin or kidney ischemia molecule-1 mRNA. Hematoxylin and eosin staining revealed patchy denudation of renal epithelial cells and tubular dilation when NFAT5 was silenced. The number of TUNEL-positive cells in the outer and inner medulla of the clamped kidney increased nearly 2-fold after knockdown of NFAT5 and was associated with an increase in the number of caspase-3-positive cells. Collectively, the data suggest that NFAT5 is part of a protective mechanism that limits renal damage induced by IRI.
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Registered trials
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