ArticleScientific reports2021
Cigarette smoke extract and heated tobacco products promote ferritin cleavage and iron accumulation in human corneal epithelial cells.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 28 citations in OpenAlex.
- Review
- Indoor Environmental Exposures and Dry Eye Disease: Mechanisms, Clinical Impact, and Prevention Strategies.Toxics · 2026Review
- Metal ions in aging and ocular diseases: biology, pathophysiology, and therapeutic strategies.npj aging · 2026Review
- Effect of I Quit Ordinary Smoking (IQOS) Use on Hepcidin and Iron Parameters in Comparison with Conventional Smoking.Iranian journal of public health · 2025Article
- Ferroptosis and organelle roles in dry eye.iScience · 2025Review
- A Bioengineered Model of the Human Cornea for Preclinical Assessment of Human Ocular Exposure to Environmental Toxicants.Advanced healthcare materials · 2025Article
- Redefining cell death: ferroptosis as a game-changer in ophthalmology.Frontiers in immunology · 2025Review
- Cigarette smoke extract induces ferroptosis in human retinal pigment epithelial cells.Heliyon · 2024Article
- Review
- Ferroptosis as a Potential Therapeutic Target for Reducing Inflammation and Corneal Scarring in Bacterial Keratitis.Investigative ophthalmology & visual science · 2024Article
- Delphinidins from Maqui Berry (Aristotelia chilensis) ameliorate the subcellular organelle damage induced by blue light exposure in murine photoreceptor-derived cells.BMC complementary medicine and therapies · 2024Article
- Inhalation of nicotine-containing electronic cigarette vapor exacerbates the features of COPD by inducing ferroptosis in βENaC-overexpressing mice.Frontiers in immunology · 2024Article
- A scoping review of the toxicity and health impact of IQOS.Tobacco induced diseases · 2024Article
- Ferroptosis: a novel mechanism of cell death in ophthalmic conditions.Frontiers in immunology · 2024Review
- Ferroptosis: mechanisms and advances in ocular diseases.Molecular and cellular biochemistry · 2023Review
- Nature-Inspired Bioactive Compounds: A Promising Approach for Ferroptosis-Linked Human Diseases?Molecules (Basel, Switzerland) · 2023Review
- Article
- Silencing USP19 alleviates cigarette smoke extract-induced mitochondrial dysfunction in BEAS-2B cells by targeting FUNDC1.Open medicine (Warsaw, Poland) · 2023Article
- A Novel Ferroptosis Inhibitor UAMC-3203, a Potential Treatment for Corneal Epithelial Wound.Pharmaceutics · 2022Article
- Autophagy in the normal and diseased cornea.Experimental eye research · 2022Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The cornea is directly exposed to cigarette smoke, and smoking is a risk factor for several corneal diseases including dry eye syndrome. Currently, heated tobacco products (HTPs) are widely used as substitutes for cigarette smoking around the world. In the present study, we investigated the molecular mechanism(s) leading to cellular injury induced by cigarette smoke extract (CSE) or HTPs. Exposure to CSE perturbed the formation of tight junctions, leading to an increase in cell volume, a decrease in transepithelial electrical resistance (TER) in the human corneal epithelial cell-transformed (HCE-T) cell line. Moreover, CSE exposure induced both lipid peroxidation and ferrous [Fe(II)] ion accumulation in autolysosomal compartments. Interestingly, a cleaved form of ferritin appeared when HCE-T cells were incubated with CSE. This aberrant ferritin processing was suppressed by treatment with autophagy inhibitors. Furthermore, the CSE-induced cell death was suppressed by either ferrostatin-1 or deferoxamine (DFO). CSE exposure also promoted the expression of cytokines whereas DFO treatment inhibited the CSE-induced expression of these cytokines. Exposure to HTPs also induced both HCE-T cell death and cleaved ferritin accumulation in a concentration- and time-dependent manner. These results indicated that CSE or HTPs activated the ferroptosis signaling pathway, which contributed to corneal epithelial cell injury.
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