ArticleAging and disease2022
MiR-29a-3p Improves Acute Lung Injury by Reducing Alveolar Epithelial Cell PANoptosis.
Article in Aging and disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.
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Who cites it
86 citing papers in PubMed, 153 citations in OpenAlex.
- Targeting the non-coding RNA-PANoptosis axis: a novel frontier in disease diagnosis and therapy.Apoptosis : an international journal on programmed cell death · 2026Review
- Shh-S100A10 axis curbs neuronal PANoptosis after ischemic stroke.Neural regeneration research · 2026Article
- Plants and Plant-Derived Compounds Mediate Protection Across Diverse Pathological Conditions by Targeting the PANoptosis Pathways.Phytotherapy research : PTR · 2026Review
- Salvianolic Acid A Relieves Acute Lung Injury by Promoting the Expression of FOXO1 and Activating Autophagy Through the Inhibition of miR-217-5p.Biochemical genetics · 2026Article
- PANoptosis and Immune Remodeling in the Tumor Microenvironment.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Review
- The potential clinical value of combining serum miR-769-5p with lung ultrasound for the diagnosis of acute lung injury.Journal of cardiothoracic surgery · 2026Article
- GPR84 aggravates lung inflammation through activating ZBP1-PANoptosome mediated PANoptosis following IAV infection.Cell death discovery · 2026Article
- Treating acute respiratory distress syndrome with a multifaceted nanomedicine: Inhibition of PANoptosis and enhancement of lung barrier integrity.Materials today. Bio · 2026Article
- N6-methyladenosine methylation in acute lung injury: Mechanisms and research progress.Journal of intensive medicine · 2026Review
- Suppression of endothelial cell PANoptosis: qingyi decoction targets the TMAO-HMGB1 pathway to mitigate lung injury in acute pancreatitis rats.Apoptosis : an international journal on programmed cell death · 2026Article
- Neutrophil-macrophage crosstalk network in acute lung injury: feedback circuits linking cytokine storm and cell death.Frontiers in cellular and infection microbiology · 2026Review
- Circulating and Respiratory Biomarkers in Sepsis-Induced ARDS: Diagnostic and Prognostic Insights - A Narrative Review.Journal of inflammation research · 2026Review
- Golgi-Targeted Viscosity Fluorescent Probe for Monitoring Acute Lung Injury.Chemistry (Weinheim an der Bergstrasse, Germany) · 2025Article
- Mitochondria at the intersections of RNA modifications and metabolism reprogramming implications in cell death, tumor microenvironment, and immunotherapy.Journal of hematology & oncology · 2025Review
- Targeting PANoptosis: a promising therapeutic strategy for ALI/ARDS.Apoptosis : an international journal on programmed cell death · 2025Review
- miR-29a-3p serves as a potential biomarker for diagnosing spinal tuberculosis: a comprehensive analysis integrating clinical data and molecular markers.BMC musculoskeletal disorders · 2025Article
- Epigallocatechin-3-gallate ameliorates lipopolysaccharide-induced inflammation via the 67LR/JAK2/STAT3 signaling pathway.Scientific reports · 2025Article
- Advances inMicroorganisms · 2025Review
- ALKBH5 suppresses miR-29a-3p expression, thereby exacerbating the inflammatory response associated with spinal tuberculosis.Journal of orthopaedic surgery and research · 2025Article
- Transcriptome sequencing showed the differential expression of circRNAs in human pulmonary microvascular endothelial cells in acute respiratory distress syndrome.Journal of thoracic disease · 2025Article
26 more citing papers are in PubMed but not listed here.
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Authors and funding
20 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alveolar epithelial cell damage is an important determinant of the severity of acute lung injury/acute respiratory distress syndrome (ALI/ARDS). However, the molecular mechanisms of alveolar epithelial death during the development of ALI/ARDS remain unclear. In this study, we explore the role of miR-29a-3p in ALI/ARDS and its molecular mechanism. Plasma samples were collected from healthy controls and ARDS patients. Mice were intratracheally instilled with lipopolysaccharide (LPS) to establish acute lung injury. N6-adenosine (m6A) quantification, RNA-binding protein immunoprecipitation, cell viability assay, quantitative real-time polymerase chain reaction, and western blotting were performed. We found that miR-29a-3p was down-regulated in plasma of ARDS patients and lung tissue of ALI model mice, and miR-29a-3p agomir injection down-regulated the levels of the inflammatory factors, including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) in the lungs, reducing alveolar epithelial cell PANoptosis as evaluated by the downregulation of Z-DNA binding protein 1 (ZBP1), gasdermin D (GSDMD), caspase-3, caspase-8, and mixed lineage kinase domain-like protein (MLKL), ultimately improving lung injury in the ALI model mice. Mechanism studies demonstrated that the knockout of methyltransferase 3 (N6-adenosine-methyltransferase complex catalytic subunit) removed the m6A modification of miR-29a-3p and reduced miR-29a-3p expression. Our findings suggest that miR-29a-3p is a potential target that can be manipulated for ALI/ARDS.
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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.