ReviewFrontiers in pharmacology2024
Role and mechanisms of autophagy, ferroptosis, and pyroptosis in sepsis-induced acute lung injury.
Review in Frontiers in pharmacology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed.
- LAPTM5 Downregulation-Driven VAMP8 Phosphorylation Impairs Autophagosome-Lysosome Fusion and Aggravates Septic Acute Lung Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Salvianolic Acid B Inhibits Ferroptosis in Acute Lung Injury: Network Analysis and Experimental Validation.Journal of cellular and molecular medicine · 2026Article
- Review
- Ferroptosis-Senescence Crosstalk in Sepsis-Associated Acute Lung Injury: Mechanisms and Therapeutic Opportunities.Biomedicines · 2026Review
- The role of cellular senescence in sepsis and its mechanism in copper death: An analysis based on machine learning.Medicine · 2026Article
- circGAB1 Activates Autophagy to Promote Sepsis-Associated Acute Kidney Injury by Interacting with ELAVL1 to Activate the HMGB3/β-catenin Signaling Pathway.Applied biochemistry and biotechnology · 2026Article
- Clinical implications of ferroptosis in critical illness: a narrative review.Journal of intensive care · 2026Review
- Meloxicam Alleviates Sepsis-Induced Lung Injury by Inhibiting Pyroptosis Through CBP/TXNIP/p38 Signaling Pathway.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Autophagy-epithelial-mesenchymal transition crosstalk in acute respiratory distress syndrome: Mechanistic insights and therapeutic perspectives (Review).Experimental and therapeutic medicine · 2026Review
- An immune-mediated effect of the antibiotic cefiderocol on LPS-induced acute lung injury.Antimicrobial agents and chemotherapy · 2026Article
- Autophagy-ferroptosis crosstalk in sepsis: metabolic pathways, redox injury, and host-directed antioxidant nanomedicine.Frontiers in immunology · 2026Review
- Sivelestat sodium alleviates sepsis-associated acute lung injury by inhibiting ferroptosis via the Nrf2/SLC7A11/GPX4 axis.PloS one · 2026Article
- Neutrophil-macrophage crosstalk network in acute lung injury: feedback circuits linking cytokine storm and cell death.Frontiers in cellular and infection microbiology · 2026Review
- TET2: a critical regulatory hub with broad therapeutic implications across human diseases.Frontiers in immunology · 2026Review
- Pathological networks and multi-target interventions in sepsis-associated acute lung injury: from pathogen-host interactions to gut-lung axis regulation.Frontiers in immunology · 2026Review
- Demethoxycurcumin Alleviates Lipopolysaccharide-Induced Acute Lung Injury via Nrf2-Mediated Anti-Inflammation and Ferroptosis Inhibition.Mediators of inflammation · 2026Article
- Adipose-derived mesenchymal stem cell-exosomes attenuate lipopolysaccharide-induced acute lung injury in mice by regulating the TGFBR2/Smad4 axis to suppress NLRP3-mediated macrophage M1 polarization and pyroptosis.Frontiers in immunology · 2026Article
- Ferroptosis in smoke inhalation injury: from mechanisms to potential therapeutic targets.Frontiers in cell and developmental biology · 2026Review
- FGF2 alleviates LPS-induced acute lung injury by inhibiting ferritinophagy-mediated ferroptosis in AT2 cells via the Hippo-YAP signaling pathway.Frontiers in immunology · 2026Article
- A dihydrofuro[2,3-b] benzofuran derivative alleviates lipopolysaccharide induced acute lung injuryFrontiers in pharmacology · 2026Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis-induced acute lung injury (ALI) is a major cause of death among patients with sepsis in intensive care units. By analyzing a model of sepsis-induced ALI using lipopolysaccharide (LPS) and cecal ligation and puncture (CLP), treatment methods and strategies to protect against ALI were discussed, which could provide an experimental basis for the clinical treatment of sepsis-induced ALI. Recent studies have found that an imbalance in autophagy, ferroptosis, and pyroptosis is a key mechanism that triggers sepsis-induced ALI, and regulating these death mechanisms can improve lung injuries caused by LPS or CLP. This article summarized and reviewed the mechanisms and regulatory networks of autophagy, ferroptosis, and pyroptosis and their important roles in the process of LPS/CLP-induced ALI in sepsis, discusses the possible targeted drugs of the above mechanisms and their effects, describes their dilemma and prospects, and provides new perspectives for the future treatment of sepsis-induced ALI.
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