ArticleMedComm2023
Novel aspect of neprilysin in kidney fibrosis via ACSL4-mediated ferroptosis of tubular epithelial cells.
Article in MedComm, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed, 21 citations in OpenAlex.
- New insights into diagnostic values and mechanisms of ferroptosis associated with immune infiltration in diabetic kidney disease.Experimental and therapeutic medicine · 2026Article
- NSUN5 Attenuates Renal Injury and Ferroptosis in Hyperuricaemic Nephropathy Through YBX2-Dependent Stabilisation of SCD1 m5C Methylation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The effects of sacubitril/valsartan compared to valsartan in experimentally induced chronic kidney disease.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Benzoxazole Derivatives as Potent FXR and PPARα Dual Agonists With Anti-Fibrotic and Metabolic Regulatory Effects.MedComm · 2025Article
- Ferroptosis in Cancer and Inflammatory Diseases: Mechanisms and Therapeutic Implications.MedComm · 2025Review
- Single-cell multi-omics analysis identifies SPP1Biomarker research · 2025Article
- Self-Assembled Carrier Free Oligomeric Proanthocyanidin/Tetrandrine Nanoparticles Ameliorate Osteoarthritis via Anti-Inflammatory and Anti-Ferroptotic Pathways.International journal of nanomedicine · 2025Article
- Anthraquinones fromDrug design, development and therapy · 2025Review
- Unraveling Ferroptosis: A New Frontier in Combating Renal Fibrosis and CKD Progression.Biology · 2024Review
- Article
- Ferroptosis in organ fibrosis: From mechanisms to therapeutic medicines.Journal of translational internal medicine · 2024Article
- Comprehensive review on neprilysin (NEP) inhibitors: design, structure-activity relationships, and clinical applications.Frontiers in pharmacology · 2024Review
- Article
- Novel aspect of neprilysin in kidney fibrosis via ACSL4-mediated ferroptosis of tubular epithelial cells.MedComm · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although inhibition of neprilysin (NEP) might be a therapeutic strategy with the potential to improve the outcome of chronic kidney disease (CKD), the versatile function of NEP with its mechanism remains obscure in kidney fibrosis. In the study, we found that NEP was abnormally increased in tubular epithelial cells of CKD patients, as well as unilateral ureteral obstruction and adenine diet-induced mice. Treatment with a United States Food and Drug Administration-approved NEP inhibitor Sacubitrilat (LBQ657) could alleviate ferroptosis, tubular injury, and delay the progression of kidney fibrosis in experimental mice. Similarly, genetic knockdown of NEP also inhibited tubular injury and fibrosis in transforming growth factor (TGF)-β1 -induced tubular cells. Mechanically, NEP overexpression aggravated the ferroptotic and fibrotic phenotype, which was restored by acyl-CoA synthetase long-chain family member 4 (ACSL4) knockdown. The NEP silencing attenuated TGF-β1-induced tubular cell ferroptosis and was exacerbated by ACSL4 overexpression. Collectively, for the first time, a novel aspect of NEP was explored in kidney fibrosis through ACSL4-mediated tubular epithelial cell ferroptosis. Our data further confirmed that NEP inhibition exerted a promising therapeutic against fibrotic kidney diseases.
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.