ReviewFrontiers in physiology2025
Mechanisms of alveolar type II epithelial cells' mitochondrial quality control during acute lung injury/acute respiratory distress syndrome: bridging the gap between oxidative stress, inflammation, and fibrosis.
Review in Frontiers in physiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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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
11 citing papers in PubMed.
- OTULIN protects hyperoxia-induced neonatal lung injury and modulates mitochondrial protein OPA1 in association with the E3 ubiquitin ligase RNF31.Cellular & molecular biology letters · 2026Article
- Alveolar epithelial barrier disruption by FKBP5-mediated necroptosis aggravates lung injury.Respiratory research · 2026Article
- Review
- Adrenergic receptors: a key determinant of outcomes in bacterial pneumonia and bacterial sepsis-associated acute lung injury/acute respiratory distress syndrome through participation in pulmonary innate immune response.Frontiers in immunology · 2026Review
- Lipid droplet-mitochondria contact sites as druggable spatial-pharmacology targets in respiratory disease: cross-cell-type mechanisms and translational strategies.Frontiers in cell and developmental biology · 2026Review
- Nicotinamide adenine dinucleotide phosphate oxidase 4 in lung disease: a review of its biology and therapeutic potential.Experimental biology and medicine (Maywood, N.J.) · 2026Review
- Ferroptosis in smoke inhalation injury: from mechanisms to potential therapeutic targets.Frontiers in cell and developmental biology · 2026Review
- Novel Carbon Dots Nanomaterials for the Precision Diagnosis and Treatment of Acute Lung Injury and Acute Respiratory Distress Syndrome: Mechanisms and Applications.International journal of nanomedicine · 2026Review
- Ferroptosis suppressor protein 1-mediated ferroptosis suppression in sepsis: non-canonical antioxidant pathways, inflammatory regulation, and therapeutic perspectives.Frontiers in immunology · 2026Review
- Innate immune circuits in acute lung injury: macrophage plasticity, ILC crosstalk, and tissue repair failure.Frontiers in immunology · 2026Review
- Gut microbiota in acute lung injury/acute respiratory distress syndrome: mechanistic insights and therapeutic opportunities via the gut-lung axis.Frontiers in cellular and infection microbiology · 2026Review
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are a group of conditions characterized by acute episodes of pulmonary inflammation and increased pulmonary vascular permeability. These conditions often result in severe morbidity and high mortality rates. Increased alveolar-capillary barrier permeability is a pivotal factor in the pathogenesis of ALI/ARDS, and diffuse alveolar epithelial cell (AEC) death is a salient feature of ALI/ARDS. Alveolar epithelium is composed of alveolar type I epithelial cells (AECI) and alveolar type II epithelial cells (AECII), with AECII playing a more critical role. These cells contain a high density of mitochondria in their cytoplasm, and their function depends on mitochondrial quality control (MQC). Existing reviews either focus solely on the mechanisms of AECs and their relationship to lung injury/fibrosis or broadly explore the role of mitochondrial dynamics in lung diseases. However, neither review comprehensively addresses AECII's MQC and related molecules and signaling pathways. The objective of this study is to investigate the MQC characteristics of AECII in ALI/ARDS, elucidate their role as a regulatory hub for oxidative stress, inflammation, and fibrosis, summarize progress in related clinical trials, and highlight the need for further research to develop effective therapies.
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Registered trials
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