ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Onion-Mitochondria Inhibit Lipopolysaccharide-Induced Acute Lung Injury by Shaping Lung Macrophage Mitochondrial Function.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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.
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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.
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Who cites it
6 citing papers in PubMed.
- Mitochondria-Targeted Nanotherapeutics: A Promising Strategy in Modulating Mitochondrial Function, Transfer, and Transplantation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Review
- Mitochondrial dysfunction in ARDS: unraveling the regulatory networks and therapeutic opportunities.Frontiers in immunology · 2026Review
- Celastrol-Based Hybrid Prodrug Ameliorates ALI by Spatiotemporally Consecutive Dual-Targeting GLUT1/Drp1 to Reestablish Mitochondrial Homeostasis.International journal of biological sciences · 2026Article
- Mitochondrial quality control mechanisms as molecular targets for impaired lung development: from fetuses to neonates.Respiratory research · 2025Review
- Onion-Mitochondria Inhibit Lipopolysaccharide-Induced Acute Lung Injury by Shaping Lung Macrophage Mitochondrial Function.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
Corrections and comments
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Authors and funding
14 authors.
Funding
Abstract
Mitochondrial dysfunction contributes to various inflammatory-related diseases by triggering the release of inflammatory molecules. Targeting mitochondrial dysfunction is emerging as a promising avenue for treating inflammatory diseases. Here, it is demonstrated that dietary plant-derived mitochondria (P-Mit) are capable of rescuing the lung macrophage mitochondrial (M-Mit) dysfunction in lipopolysaccharide (LPS)-induced mouse acute lung injury (ALI). Specifically, oral administration of dietary onion-derived mitochondria (O-Mit) can travel from the gut to the lungs in ALI mice, where preferentially uptake by lung macrophage mediated by the interaction between O-Mit phosphatic acid (PA) and macrophage complement C3b/C4b receptor 1 Like (CR1L), followed by fusing with murine M-Mit and by reprograming the M-Mit energy metabolism in the lungs of ALI mice. Further evidence suggests that O-Mit enriches methyl 3,4-dihydroxybenzoate (MDHB) inhibits M-Mit NADH dehydrogenase subunit 1 (ND1) gene expression in the epigenetic process, which represses LPS-induced complex I-related oxidative stress activation and excessive mitochondrial fission via modulating dynamin-related protein 1 (DRP1) phosphorylation and cardiolipin peroxidation in M-Mit, eventually rescues the LPS-induced ALI. Given LPS-induced mouse model of ALI is widely used to study human ALI and acute respiratory distress syndrome, this finding provides a clinical potential for the treatment of human ALI via edible P-Mit.
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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.