ArticleCells2022
TMEM43 Protects against Sepsis-Induced Cardiac Injury via Inhibiting Ferroptosis in Mice.
Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 50 citations in OpenAlex.
- Ferroptosis as a target mechanism in heart and kidney disease.The Journal of clinical investigation · 2026Review
- Research Progress on the Role of Traditional Chinese Medicine in Regulating Ferroptosis in Cardiovascular Diseases.Biology · 2026Review
- Inhibition of iron overload and ferroptosis attenuates sepsis-induced myocardial injury in mice through STAT3/Lcn2 pathway.Journal of cardiothoracic surgery · 2026Article
- Integrative transcriptome and microbiome analysis reveals ferroptosis-driven duodenal damage caused by Ochratoxin A in mice.Frontiers in immunology · 2026Article
- Targeting ferroptosis in sepsis-induced cardiomyopathy: mechanisms and therapeutic potential of traditional Chinese Medicine.Frontiers in pharmacology · 2026Review
- Early Postnatal Stress as a Risk Factor for Cardiac Pathology in Systemic Inflammatory Conditions: An Experimental Study.Bulletin of experimental biology and medicine · 2025Article
- HIPK2 Confers Protection Against Septic Myocardial Injury by Regulating Ferroptosis.Cardiovascular toxicology · 2025Article
- Targeting ATF4-DDIT4/TXNIP induced mitochondrial dysfunction and ferroptosis: ISRIB as novel therapy for septic cardiomyopathy.Journal of translational medicine · 2025Article
- Transmembrane Protein 43: Molecular and Pathogenetic Implications in Arrhythmogenic Cardiomyopathy and Various Other Diseases.International journal of molecular sciences · 2025Review
- New developments in the role of ferroptosis in sepsis‑induced cardiomyopathy (Review).Molecular medicine reports · 2025Review
- Overexpression of Wild-Type TMEM43 Improves Cardiac Function in Arrhythmogenic Right Ventricular Cardiomyopathy Type 5.Circulation research · 2025Article
- P53 Regulation upon Lipid Peroxidation and Ferroptosis for Intervention against Atherogenesis.Current medicinal chemistry · 2025Review
- Ferroptosis: The Pivotal Link in Cardiovascular Diseases Pathogenesis and Therapy.International journal of general medicine · 2025Review
- Glycine attenuates sepsis-induced white matter injury by modulating gut microbiota.Frontiers in molecular biosciences · 2025Article
- The Effect of Hydroxysafflor Yellow A on Inflammatory Injury in LPS-induced Endothelial Cell Injury Model through TLR4/NF-κB Pathway Based on Network Pharmacology and Experimental Verification.Current pharmaceutical biotechnology · 2025Article
- Minocycline alleviates lipopolysaccharide-induced cardiotoxicity by suppressing the NLRP3/Caspase-1 signaling pathway.Scientific reports · 2024Article
- TMEM100 acts as a TAK1 receptor that prevents pathological cardiac hypertrophy progression.Cell communication and signaling : CCS · 2024Article
- Ferroptosis mechanisms and regulations in cardiovascular diseases in the past, present, and future.Cell biology and toxicology · 2024Review
- Ferroptosisand Its Role in the Treatment of Sepsis-Related Organ Injury: Mechanisms and Potential Therapeutic Approaches.Infection and drug resistance · 2024Review
- Propofol and Dexmedetomidine Ameliorate Endotoxemia-Associated Encephalopathy via Inhibiting Ferroptosis.Drug design, development and therapy · 2024Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A previous study found that transmembrane protein 43 (TMEM43) was highly associated with arrhythmogenic right ventricular dysplasia/cardiomyopathy. However, as a transmembrane protein, TMEM43 may be involved in ferroptosis in cardiovascular disease. In this study, we aimed to explore the role of TMEM43 in lipopolysaccharide (LPS)-induced cardiac injury and the underlying mechanism. Mice were injected with LPS (10 mg/kg) for 12 h to generate experimental sepsis. Mice were also subjected to AAV9-shTMEM43 to knock down TMEM43 or AAV9-TMEM43 to overexpress TMEM43 in hearts. H9c2 rat cardiomyocytes were also transfected with Ad-TMEM43 or TMEM43 siRNA to overexpress/knock down TMEM43. As a result, TMEM43 knockdown in hearts deteriorated LPS-induced mouse cardiac injury and dysfunction. LPS increased cardiac ferroptosis as assessed by malonaldehyde (MDA) and cardiac iron density, which were aggravated by TMEM43 knockdown. Moreover, TMEM43 overexpression alleviated LPS-induced cardiac injury, dysfunction, and ferroptosis. In vitro experiments showed that TMEM43 overexpression inhibited LPS-induced lipid peroxidation and cardiomyocyte injury while TMEM43 knockdown aggravated LPS-induced ferroptosis and injury in cardiomyocytes. Mechanistically, LPS increased the expression of P53 and ferritin but decreased the level of Gpx4 and SLC7A11. TMEM43 could inhibit the level of P53 and ferritin enhanced the level of Gpx4 and SLC7A11. Furthermore, ferrostatin-1 (Fer-1), a specific inhibitor of ferroptosis, could protect against LPS-induced cardiac injury and also counteracted the deteriorating effects of TMEM43 silencing in the heart. Based on these findings, we concluded that TMEM43 protects against sepsis-induced cardiac injury via inhibiting ferroptosis in mice. By targeting ferroptosis in cardiomyocytes, TMEM43 may be a therapeutic strategy for preventing sepsis in the future.
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