ArticleCommunications biology2023
Inhibition of ACSL4 ameliorates tubular ferroptotic cell death and protects against fibrotic kidney disease.
Article in Communications biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 62 citations in OpenAlex.
- Mitochondrial dysfunction-ferroptosis crosstalk drives renal fibrosis in chronic kidney disease.Renal failure · 2026Review
- Ferroptosis and Ferro-Aging in Obesity: Bibliometric Mapping, Shared Mechanisms, and Translational Perspectives.Metabolites · 2026Review
- Ferroptosis in kidney disease.Nature reviews. Nephrology · 2026Review
- SOCS2 Downregulation Is Associated with a Ferro-Aging-Related Transcriptomic Signature in Proximal Tubular Cells in Chronic Kidney Disease.Biomedicines · 2026Article
- Repurposing approved drugs as ferroptosis modulators: a critical review of clinical trials in cancer and neurodegeneration.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Organelle Crosstalk in Renal Cells: Insights from Cell Biology and Implications for AKI-to-CKD Transition.International journal of molecular sciences · 2026Review
- Metabolic regulation of ferroptosis in cancer: mechanisms, pharmacological inducers, and translational challenges.Apoptosis : an international journal on programmed cell death · 2026Review
- Monocyte-Derived Macrophage Ferroptosis Amplifies Cholangitis in Primary Biliary Cholangitis via a Calpain/ACSL4 Axis.Biomedicines · 2026Article
- Small molecules targeting regulated cell death for chronic kidney disease therapy.Journal of pharmaceutical analysis · 2026Review
- Ferroptosis in Recurrent Vulvovaginal Candidiasis Through Integrated Bioinformatics and Experimental Validation.Antioxidants (Basel, Switzerland) · 2026Article
- ACSL4 mediates ferroptosis to promote immunoglobulin A nephropathy progression: scRNA-seq analysis.Scientific reports · 2026Article
- Ferroptosis and immunity: rewiring the tumor microenvironment for therapy.RSC advances · 2026Review
- Huaier Aqueous Extract Combined with Gefitinib Promotes ACSL4-Dependent Ferroptosis and Overcomes Gefitinib Resistance in Non-Small Cell Lung Cancer.Current medical science · 2026Article
- 6-Gingerol Regulates the Exosomal miR-148b-3p/ACSL4/Ferroptosis Axis in an in vitro Model of Diabetic Retinopathy.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Article
- Renal allograft interstitial fibrosis: multicellular interactions and therapeutic strategies.Frontiers in immunology · 2026Review
- Iron metabolism and ferroptosis: druggable targets to delay the progression of lupus nephritis.American journal of physiology. Renal physiology · 2026Review
- HPDA-based tubule-targeting nanoplatform alleviates oxidative stress and ferroptosis for the reversal of renal interstitial fibrosis.Journal of nanobiotechnology · 2025Article
- Protective effects and mechanisms of cynaroside on renal fibrosis in mice with unilateral ureteral obstruction.Redox report : communications in free radical research · 2025Article
- March6 Protects Against Acute Kidney Injury by Suppressing Renal Tubular Epithelial Cell Ferroptosis Through the Destabilization of P53 and ACSL4 Proteins.Inflammation · 2025Article
- Ferroptosis and renal fibrosis: mechanistic insights and emerging therapeutic targets.Renal failure · 2025Review
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ferroptosis is a recently recognized form of regulated cell death, characterized by iron-dependent accumulation of lipid peroxidation. Ample evidence has depicted that ferroptosis plays an essential role in the cause or consequence of human diseases, including cancer, neurodegenerative disease and acute kidney injury. However, the exact role and underlying mechanism of ferroptosis in fibrotic kidney remain unknown. Acyl-CoA synthetase long-chain family member 4 (ACSL4) has been demonstrated as an essential component in ferroptosis execution by shaping lipid composition. In this study, we aim to discuss the potential role and underlying mechanism of ACSL4-mediated ferroptosis of tubular epithelial cells (TECs) during renal fibrosis. The unbiased gene expression studies showed that ACSL4 expression was tightly associated with decreased renal function and the progression of renal fibrosis. To explore the role of ACSL4 in fibrotic kidney, ACSL4 specific inhibitor rosiglitazone (ROSI) was used to disturb the high expression of ACSL4 in TECs induced by TGF-β, unilateral ureteral obstruction (UUO) and fatty acid (FA)-modeled mice in vivo, and ACSL4 siRNA was used to knockdown ACSL4 in TGF-β-induced HK2 cells in vitro. The results demonstrated that inhibition and knockdown of ACSL4 effectively attenuated the occurrence of ferroptosis in TECs and alleviated the interstitial fibrotic response. In addition, the expression of various profibrotic cytokines all decreased after ROSI-treated in vivo and in vitro. Further investigation showed that inhibition of ACSL4 obviously attenuates the progression of renal fibrosis by reducing the proferroptotic precursors arachidonic acid- and adrenic acid- containing phosphatidylethanolamine (AA-PE and AdA-PE). In conclusion, these results suggest ACSL4 is essential for tubular ferroptotic death during kidney fibrosis development and ACSL4 inhibition is a viable therapeutic approach to preventing fibrotic kidney diseases.
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