ArticleAmerican journal of respiratory cell and molecular biology2024
The Regulation of Fatty Acid Synthase by Exosomal miR-143-5p and miR-342-5p in Idiopathic Pulmonary Fibrosis.
Article in American journal of respiratory cell and molecular biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 25 citations in OpenAlex.
- How extracellular vesicles contribute to pulmonary fibrosis: miRNA-mediated mechanisms, diagnostic potential, and emerging therapeutic strategies.Molecular biology reports · 2026Review
- Exploring the role of circRNA-miRNA-mRNA interactions in cervical cancer progression: insights into HPV status and potential therapeutic approaches.Journal of applied genetics · 2026Article
- Stiffness-dependent alveolar type II cell senescence in idiopathic pulmonary fibrosis.Cell communication and signaling : CCS · 2026Article
- Freezing shock monocytes deliver antisense oligonucleotides via liposomes for the treatment of idiopathic pulmonary fibrosis.Asian journal of pharmaceutical sciences · 2026Article
- Diagnostic and therapeutic significance of exosomal miR-143-5p in the plasma of patients with rheumatoid arthritis.European journal of medical research · 2026Article
- Engineered MSC-Exosomes Delivering miRNAs for Respiratory Disease Diagnostics and Therapy: Opportunities and Challenges.International journal of nanomedicine · 2026Review
- The relationship between serum levels of miR-342 and miR-148a and acute lung injury in sepsis patients.Open medicine (Warsaw, Poland) · 2026Article
- Lipid metabolism as a cell-state determinant in pulmonary fibrosis: from epithelial failure to ferroptosis-driven amplification.Frontiers in pharmacology · 2026Review
- MiR-143-5p serves as a diagnostic biomarker in patients with sepsis and regulates sepsis-induced inflammation and cardiac dysfunction.Hereditas · 2025Article
- The mechanism of plasma exosome miR-15a-5p targeting the CF-modified protein IGF1R to regulate alveolar epithelial autophagy and influence pulmonary interstitial fibrosis.Non-coding RNA research · 2025Article
- Variable steady inflammation and inflammatory responses in precision-cut lung slices from various IPF lung Regions.Respiratory research · 2025Article
- Construction of a nomogram model for individualized prediction of extracorporeal membrane oxygenation weaning outcomes in cardiogenic shock.BMC cardiovascular disorders · 2025Article
- Engineerable mesenchymal stem cell-derived extracellular vesicles as promising therapeutic strategies for pulmonary fibrosis.Stem cell research & therapy · 2025Review
- Idiopathic Pulmonary Fibrosis Caused by Damaged Mitochondria and Imbalanced Protein Homeostasis in Alveolar Epithelial Type II Cell.Advanced biology · 2025Review
- Review
- Fatty acid synthase inhibition alleviates lung fibrosis via β-catenin signal in fibroblasts.Life science alliance · 2025Article
- Ferroptosis in idiopathic pulmonary fibrosis: mechanisms, impact, and therapeutic opportunities.Frontiers in immunology · 2025Review
- miR-335-5p Predicts Elevated Chronic Obstructive Pulmonary Disease (COPD) Susceptibility and Its Role in Human Bronchial Epithelial Cells Injury.International journal of chronic obstructive pulmonary disease · 2025Article
- What do we know about extracellular vesicles in patients with idiopathic pulmonary fibrosis? a scoping review.Frontiers in immunology · 2025Article
- Emerging roles of noncoding RNAs in idiopathic pulmonary fibrosis.Cell death discovery · 2024Review
Corrections and comments
- Commented on by
Authors and funding
11 authors at 4 institutions in 4 countries.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) is a chronic and progressive disease caused by an aberrant repair of injured alveolar epithelial cells. The maintenance of the alveolar epithelium and its regeneration after the damage is fueled by alveolar type II (ATII) cells. Injured cells release exosomes containing microRNAs (miRNAs), which can alter the recipient cells' function. Lung tissue, ATII cells, fibroblasts, plasma, and exosomes were obtained from naive patients with IPF, patients with IPF taking pirfenidone or nintedanib, and control organ donors. miRNA expression was analyzed to study their impact on exosome-mediated effects in IPF. High miR-143-5p and miR-342-5p levels were detected in ATII cells, lung tissue, plasma, and exosomes in naive patients with IPF. Decreased FASN (fatty acid synthase) and ACSL-4 (acyl-CoA-synthetase long-chain family member 4) expression was found in ATII cells. miR-143-5p and miR-342-5p overexpression or ATII cell treatment with IPF-derived exosomes containing these miRNAs lowered FASN and ACSL-4 levels. Also, this contributed to ATII cell injury and senescence. However, exosomes isolated from patients with IPF taking nintedanib or pirfenidone increased FASN expression in ATII cells compared with naive patients with IPF. Furthermore, fibroblast treatment with exosomes obtained from naive patients with IPF increased SMAD3, CTGF, COL3A1, and TGFβ1 expression. Our results suggest that IPF-derived exosomes containing miR-143-5p and miR-342-5p inhibited the
Indexed as
Identifiers
What OpenQuestion holds
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.