ArticleFrontiers in pharmacology2018
Pharmacological Inhibition of Fatty Acid-Binding Protein 4 (FABP4) Protects Against Rhabdomyolysis-Induced Acute Kidney Injury.
Article in Frontiers in pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 28 citations in OpenAlex.
- Fatty Acid-Binding Proteins and Substance Use Disorders: From Lipid Signaling to Therapeutic Targets.Genes · 2026Review
- The Regulatory Role of FABP4 in Microbiome-Brain-Gut Communication Under High-Fat-Diet Conditions.International journal of molecular sciences · 2026Review
- Fatty acid-binding protein-3 and renal function decline in patients with chronic coronary syndrome.Clinical cardiology · 2024Article
- Vitamin D receptor attenuate ischemia-reperfusion kidney injury via inhibiting ATF4.Cell death discovery · 2023Article
- Fatty acid-binding protein 4 is a therapeutic target for septic acute kidney injury by regulating inflammatory response and cell apoptosis.Cell death & disease · 2022Article
- Fatty Acid β-Oxidation in Kidney Diseases: Perspectives on Pathophysiological Mechanisms and Therapeutic Opportunities.Frontiers in pharmacology · 2022Review
- Pre-emptive pharmacological inhibition of fatty acid-binding protein 4 attenuates kidney fibrosis by reprogramming tubular lipid metabolism.Cell death & disease · 2021Article
- Lipidomics Provides New Insight into Pathogenesis and Therapeutic Targets of the Ischemia-Reperfusion Injury.International journal of molecular sciences · 2021Review
- Activation of aryl hydrocarbon receptor by 6-formylindolo[3,2-b]carbazole alleviated acute kidney injury by repressing inflammation and apoptosis.Journal of cellular and molecular medicine · 2021Article
- Comprehensive Analysis of the Profiles of Differentially Expressed mRNAs, lncRNAs, and circRNAs in Phosgene-Induced Acute Lung Injury.BioMed research international · 2021Article
- Inhibition of Fatty Acid-Binding Protein 4 Attenuated Kidney Fibrosis by Mediating Macrophage-to-Myofibroblast Transition.Frontiers in immunology · 2020Article
- Effects of ASC Application on Endplate Regeneration Upon Glycerol-Induced Muscle Damage.Frontiers in molecular neuroscience · 2020Article
- Pharmacological and genetic inhibition of fatty acid-binding protein 4 alleviated cisplatin-induced acute kidney injury.Journal of cellular and molecular medicine · 2019Article
- Loganetin protects against rhabdomyolysis-induced acute kidney injury by modulating the toll-like receptor 4 signalling pathway.British journal of pharmacology · 2019Article
- Inhibition of Mitofusin-2 Promotes Cardiac Fibroblast Activation via the PERK/ATF4 Pathway and Reactive Oxygen Species.Oxidative medicine and cellular longevity · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute kidney injury (AKI) is a common and potentially life-threatening complication. Studies confirmed that circulating FABP4 depended on renal function of AKI patients. In our previous study, FABP4 was involved in the pathogenesis of I/R-induced AKI. However, the function of FABP4 in rhabdomyolysis-induced AKI remained poorly understood. In the study, we further investigated the effect of FABP4 in a murine model of glycerol injection-induced rhabdomyolysis. Following glycerol injection, the mice developed severe AKI as indicated by acute renal dysfunction and histologic changes, companied by the increased FABP4 expression in the cytoplasm of tubular epithelial cells. Pharmacological inhibition of FABP4 by a highly selective inhibitor BMS309403 significantly reduced serum creatinine level, proinflammatory cytokine mRNA expression of tumor necrosis factor-α, interleukin-6, and monocyte chemoattractant protein 1 as well as attenuated renal tubular damage in glycerol-injured kidneys. Oral administration of FABP4 inhibitor also resulted in a significant attenuation of ER stress indicated by transmission electron microscope analysis and its maker proteins expression of GRP78, CHOP, p-perk, and ATF4 in kidneys of AKI. Furthermore, BMS309403 could attenuate myoglobin-induced ER stress and inflammation in renal proximal tubular epithelial cell line (HK-2). Overall, these data highlighted that renal protection of selective FABP4 inhibitor was substantiated by the reduction of ER stress and inflammation in tubular epithelial cells of rhabdomyolysis-induced injured kidneys and suggested that the inhibition of FABP4 might be a promising therapeutic strategy for AKI treatment.
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.