ArticleCell death & disease2019
FABP4 contributes to renal interstitial fibrosis via mediating inflammation and lipid metabolism.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 56 citations in OpenAlex.
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- Proteomics reveals defective peroxisomal fatty acid oxidation during the progression of acute kidney injury and repair.Heliyon · 2023Article
- Role and significance of SIRT1 in regulating the LPS-activated pyroptosis pathway in children with congenital hydronephrosis.World journal of pediatric surgery · 2023Article
- Interleukin-4-induced FABP4 promotes lipogenesis in human skeletal muscle cells by activating the PPAR γ signaling pathway.Cell biochemistry and biophysics · 2022Article
- FABP4 in obesity-associated carcinogenesis: Novel insights into mechanisms and therapeutic implications.Frontiers in molecular biosciences · 2022Review
- AKT/foxo3a signal pathway mediates the protective mechanism of resveratrol on renal interstitial fibrosis and oxidative stress in rats with unilateral ureteral obstruction.American journal of translational research · 2022Article
- Therapeutic Implications of FABP4 in Cancer: An Emerging Target to Tackle Cancer.Frontiers in pharmacology · 2022Review
- The mechanism exploration of the non-colonic toxicity and obesity inhibition of food-grade κ-carrageenan by transcriptome.Food science & nutrition · 2021Article
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- Proteomic analysis of machine perfusion solution from brain dead donor kidneys reveals that elevated complement, cytoskeleton and lipid metabolism proteins are associated with 1-year outcome.Transplant international : official journal of the European Society for Organ Transplantation · 2021Article
- Pre-emptive pharmacological inhibition of fatty acid-binding protein 4 attenuates kidney fibrosis by reprogramming tubular lipid metabolism.Cell death & disease · 2021Article
- Transcriptomic analysis identifies upregulation of secreted phosphoprotein 1 in silicotic rats.Experimental and therapeutic medicine · 2021Article
- Effect of Add-On Therapy of Sodium-Glucose Cotransporter 2 Inhibitors and Dipeptidyl Peptidase 4 Inhibitors on Adipokines in Type 2 Diabetes Mellitus.Journal of clinical medicine research · 2021Article
- Fatty acid-binding protein 4 silencing protects against lipopolysaccharide-induced cardiomyocyte hypertrophy and apoptosis by inhibiting the Toll-like receptor 4-nuclear factor-κB pathway.The Journal of international medical research · 2021Article
- FABP4 alleviates endoplasmic reticulum stress-mediated ischemia-reperfusion injury in PC12 cells via regulation of PPARγ.Experimental and therapeutic medicine · 2021Article
- Low Molecular Weight Fucoidan Can Inhibit the Fibrosis of Diabetic Kidneys by Regulating the Kidney Lipid Metabolism.Journal of diabetes research · 2021Article
- GADD45α drives brown adipose tissue formation through upregulating PPARγ in mice.Cell death & disease · 2020Article
- Inhibition of Fatty Acid-Binding Protein 4 Attenuated Kidney Fibrosis by Mediating Macrophage-to-Myofibroblast Transition.Frontiers in immunology · 2020Article
Corrections and comments
- Retraction · 2021-08-20Error in Image · Investigation by Company/Institution · Manipulation of Images · Unreliable Results and/or Conclusions · · see also: https://pubpeer.com/publications/630CC3A7328E8123884CB5FA2A7AC8
- Retracted
Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fatty acid binding protein 4 (FABP4), a subtype of fatty acid-binding protein family, shows critical roles in metabolism and inflammation. However, its roles on regulating renal interstitial fibrosis (RIF) remain unclear. In this work, LPS-stimulated in vitro models on NRK-52E and NRK-49F cells, and in vivo UUO models in rats and mice were established. The results showed that comparing with control groups or sham groups, the expression levels of α-SMA, COL1A, COL3A, IL-1β, IL-6, and TNF-α in LPS-stimulated cells or UUO animals were significantly increased. Meanwhile, the levels of TC, TG, and free fatty acid were also significantly increased as well as the obvious lipid droplets, and the serum levels of BUN, Cr were significantly increased with large amounts of collagen deposition in renal tissues. Further investigation showed that compared with control groups or sham groups, the expression levels of FABP4 in LPS-stimulated cells and UUO animals were significantly increased, resulting in down- regulating the expression levels of PPARγ, upregulating the levels of p65 and ICAM-1, and decreasing the expression levels of ACADM, ACADL, SCP-2, CPT1, EHHADH, and ACOX1. To deeply explore the mechanism of FABP4 in RIF, FABP4 siRNA and inhibitor interfered cell models, and UUO model on FABP4 knockout (KO) mice were used. The results showed that the expression levels of α-SMA, COL1A, and COL3A were significantly decreased, the deposition of lipid droplets decreased, and the contents of TC, TG, and free fatty acids were significantly decreased after gene silencing. Meanwhile, the expression levels of PPAR-γ, ACADM, ACADL, SCP-2, CPT1, EHHADH, and ACOX1 were upregulated, the levels of p65 and ICAM-1 were downregulated, and the mRNA levels of IL-1β, IL-6, and TNF-α were decreased. Our results supported that FABP4 contributed to RIF via promoting inflammation and lipid metabolism, which should be considered as one new drug target to treat RIF.
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