ArticleCell death & disease2022
Inhibition of mitoNEET attenuates LPS-induced inflammation and oxidative stress.
Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 37 citations in OpenAlex.
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- Targeting macro- and micro-nutrient regulation of HNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- Non-linear relationship between serum iron levels and 28-day mortality in sepsis patients: a retrospective study.Scientific reports · 2025Observational
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- Sequentially assembled co-delivery nanoplatform of SIRT1 protein and SOX9-expressing plasmid for multipronged therapy of intervertebral disc degeneration.Journal of nanobiotechnology · 2025Article
- Macrophage A2aR Alleviates LPS-Induced Vascular Endothelial Injury and Inflammation via Inhibiting M1 Polarisation and Oxidative Stress.Journal of cellular and molecular medicine · 2025Article
- Iron-Mediated Regulation in Adipose Tissue: A Comprehensive Review of Metabolism and Physiological Effects.Current obesity reports · 2025Review
- Isolation, purification, and characterization of polysaccharides fromFrontiers in nutrition · 2025Article
- The role of mitophagy in female reproductive system diseases: from molecular mechanisms to therapeutic strategies.Frontiers in endocrinology · 2025Review
- Pharmacological Potentials and Delivery Strategies of Isoliquiritigenin: Challenges and Advances in Enhancing Bioavailability.Drug design, development and therapy · 2025Review
- Metabolic reprogramming in sepsis-associated acute kidney injury: insights from lipopolysaccharide-induced oxidative stress and amino acid dysregulation.Molecular biology reports · 2024Article
- Article
- The role of CISD1 reduction in macrophages in promoting COPD development through M1 polarization and mitochondrial dysfunction.European journal of medical research · 2024Article
- Bacterial lipopolysaccharide inhibits free thiamin uptake along the intestinal tract via interference with membrane expression of thiamin transporters 1 and 2.American journal of physiology. Cell physiology · 2024Article
- Gut microbial metabolites in MASLD: Implications of mitochondrial dysfunction in the pathogenesis and treatment.Hepatology communications · 2024Review
- CISD3/MiNT is required for complex I function, mitochondrial integrity, and skeletal muscle maintenance.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Metabolic Reprogramming and Its Regulatory Mechanism in Sepsis-Mediated Inflammation.Journal of inflammation research · 2023Review
- Identifying Protective Drugs for Parkinson's Disease in Health-Care Databases Using Machine Learning.Movement disorders : official journal of the Movement Disorder Society · 2022Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
MitoNEET (mitochondrial protein containing Asn-Glu-Glu-Thr (NEET) sequence) is a 2Fe-2S cluster-containing integral membrane protein that resides in the mitochondrial outer membrane and participates in a redox-sensitive signaling and Fe-S cluster transfer. Thus, mitoNEET is a key regulator of mitochondrial oxidative capacity and iron homeostasis. Moreover, mitochondrial dysfunction and oxidative stress play critical roles in inflammatory diseases such as sepsis. Increased iron levels mediated by mitochondrial dysfunction lead to oxidative damage and generation of reactive oxygen species (ROS). Increasing evidence suggests that targeting mitoNEET to reverse mitochondrial dysfunction deserves further investigation. However, the role of mitoNEET in inflammatory diseases is unknown. Here, we investigated the mechanism of action and function of mitoNEET during lipopolysaccharide (LPS)-induced inflammatory responses in vitro and in vivo. Levels of mitoNEET protein increased during microbial or LPS-induced sepsis. Pharmacological inhibition of mitoNEET using mitoNEET ligand-1 (NL-1) decreased the levels of pro-inflammatory cytokines such as IL-1β, IL-6, and TNF-α in animal models of sepsis, as well as LPS-induced inflammatory responses by macrophages in vitro. Inhibition of mitoNEET using NL-1 or mitoNEET shRNA abrogated LPS-induced ROS formation and mitochondrial dysfunction. Furthermore, mitochondrial iron accumulation led to generation of LPS-induced ROS, a process blocked by NL-1 or shRNA. Taken together, these data suggest that mitoNEET could be a key therapeutic molecule that targets mitochondrial dysfunction during inflammatory diseases and sepsis.
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Registered trials
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