ArticleOxidative medicine and cellular longevity2022
Adipose-Derived Circulating Exosomes Promote Protection of the Pulmonary Endothelial Barrier by Inhibiting EndMT and Oxidative Stress through Down-Regulation of the TGF-
Article in Oxidative medicine and cellular longevity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 17 citations in OpenAlex.
- Adipose-derived exosomes alleviate ALI via inhibiting epithelial-mesenchymal transition of alveolar type II cells by Wnt/β-catenin/snail pathway.Journal of translational medicine · 2026Article
- Expression of Serum and Exosomal microRNA-34a in Subjects with Increased Fat Mass.International journal of molecular sciences · 2025Article
- TET1-Mediated DNA hydroxymethylation of KLF6 promotes LPS-induced pulmonary fibrosis by activating the S1PR3/RhoA/ROCK signaling pathway.Respiratory research · 2025Article
- Inhibition of antiapoptotic BCL-2 proteins with Lipo-NPs induces fibroblast apoptosis, alleviating pulmonary fibrosis in VILI mice.Respiratory research · 2025Article
- Emerging role of exosomal-microRNA in obesity.Current opinion in physiology · 2025Article
- Catalytic neural stem cell exosomes for multi-stage targeting and synergistical therapy of retinal ischemia-reperfusion injury.Cell reports. Medicine · 2025Article
- Advances in regulating endothelial-mesenchymal transformation through exosomes.Stem cell research & therapy · 2024Review
- The Relevance of the Endothelium in Cardiopulmonary Disorders.International journal of molecular sciences · 2024Review
- Exosomes: current knowledge and future perspectives.Tissue barriers · 2024Review
- Revisiting the role of MicroRNAs in the pathogenesis of idiopathic pulmonary fibrosis.Frontiers in cell and developmental biology · 2024Review
- Deletion of thePulmonary circulation · 2023Article
- Obesity Paradox in Lung Diseases: What Explains It?Obesity facts · 2023Review
- Safety and biodistribution of exosomes derived from human induced pluripotent stem cells.Frontiers in bioengineering and biotechnology · 2022Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The "obesity paradox in acute respiratory distress syndrome" (ARDS) refers to the phenomenon in which obesity is associated with higher morbidity but lower mortality in patients with ARDS. Endothelial-to-mesenchymal transition (EndMT) represents a key link in the interaction between endothelial disruption and mesenchymal fibrosis under inflammatory and oxidative conditions, which represent the intersectional pathophysiology of ARDS. Adipose tissue is considered to constitute the major source of circulating exosomal microRNAs (miRNAs), which act as genetic forms of adipokines for cell-cell crosstalk. We aimed to demonstrate the regulation and mechanism of adipose-derived exosomes in the obesity paradox in ARDS. High-fat-induced obese mice and lean control mice were subjected to ARDS insult to investigate the effects of obesity on ARDS and microarray analysis was performed to screen for differences in circulating miRNAs. In addition, mice and pulmonary endothelial cells were administered with adipose-derived exosomal miR-122-5p to investigate the underlying molecular mechanisms. We found high-fat diet-induced obesity protected against ARDS in mice by reinforcing endothelial barrier and attenuating fibroproliferation. Circulating exosomes produced in the obese state mediated these protective effects by inhibiting EndMT and oxidative stress. Mechanistically, adipose-derived exosomal miR-122-5p promoted the integrity and function of pulmonary endothelial barrier and alleviated fibrogenesis by suppressing EndMT and oxidative stress through down-regulation of the transforming growth factor
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