ArticleAmerican journal of translational research2024
Protection against cigarette smoke-induced chronic obstructive pulmonary disease via activation of the SIRT1/FoxO1 axis by targeting microRNA-132.
Article in American journal of translational research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Association of miR-146a/b and miR-181a with Chronic Obstructive Pulmonary Disease.Biochemical genetics · 2026Article
- Exploring the anti-asthmatic effects of HMM: OVA-induced murine model and multi-target in silico analysis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Shared molecular signatures between atrial fibrillation and chronic obstructive pulmonary disease: an integrated bioinformatic analysis with experimental validation.BMC medical genomics · 2026Article
- Integrated Pulmonary Severity Score (IPSS) for COPD: A Psycho-Respiratory Risk Index Supported by Explainable Machine Learning.Diagnostics (Basel, Switzerland) · 2026Article
- The role of high-fiber diets in modulating the gut-lung axis and asthmatic inflammation.Frontiers in immunology · 2026Review
- Integrated transcriptomic and functional analysis reveals overlapping pathways in lung adenocarcinoma and chronic obstructive pulmonary disease.Hereditas · 2025Article
- Resveratrol mitigates diabetes-induced cardiac dysfunction via SIRT1/PPAR-α/PGC-1 pathway.Molecular genetics and genomics : MGG · 2025Article
- Regulatory mechanisms of luteolin in inflammatory respiratory diseases.Frontiers in pharmacology · 2025Review
- Vitamin D deficiency and asthma morbidity in school-age children: a single-center cohort study.Frontiers in public health · 2025Article
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7 authors.
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Abstract
objectiveTo investigate the biological role of miR-132 in a murine model of chronic obstructive pulmonary disease (COPD) via activation of the SIRT1/FoxO1 axis.
methodsCOPD was induced in C57BL/6J male mice by exposing them to cigarette smoke (CS) for 8 weeks. A miR-132 knockout mouse model was used to assess the role of miR-132 in CS-induced COPD. Lung tissue apoptosis was evaluated using TUNEL assays and histopathology, along with lung functional tests which were performed to assess CS-induced lung injury.
resultsElevated miR-132 expression was observed in lung tissues and bronchoalveolar lavage fluid in COPD mice. miR-132 depletion improved lung function, restored lung tissue morphology, and reduced apoptosis. Target prediction software identified miR-132 as a potential repressor of SIRT1. In COPD mice, SIRT1 and FoxO1 expression were reduced, but miR-132 knockout restored their levels.
conclusionInhibition of miR-132 may serve as a therapeutic strategy for CS-induced COPD.
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