ArticleScientific reports2016
Inhibition of autophagy ameliorates pulmonary microvascular dilation and PMVECs excessive proliferation in rat experimental hepatopulmonary syndrome.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 18 citations in OpenAlex.
- Sulfhydrated TFEB alleviates blast-induced lung injury by maintaining epithelial barrier integrity through the IGF2R/MMP-2/9 pathway.Redox biology · 2026Article
- SerpinB1a induces hepatopulmonary syndrome by promoting CTSG/AMPK/mTOR pathway-mediated mitophagy.Cell biology and toxicology · 2025Article
- Vitamin D3 improved hypoxia-induced lung injury by inhibiting the complement and coagulation cascade and autophagy pathway.BMC pulmonary medicine · 2024Article
- Glucocorticoids induce femoral head necrosis in rats through the ROS/JNK/c-Jun pathway.FEBS open bio · 2021Article
- Complex interplay between autophagy and oxidative stress in the development of pulmonary disease.Redox biology · 2020Review
- Biphasic effects of autophagy on decompression bubble-induced endothelial injury.Journal of cellular and molecular medicine · 2019Article
- Hepatocyte-derived exosomal MiR-194 activates PMVECs and promotes angiogenesis in hepatopulmonary syndrome.Cell death & disease · 2019Article
- Autophagy inhibitor 3-methyladenine protects against endothelial cell barrier dysfunction in acute lung injury.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- RAB26-dependent autophagy protects adherens junctional integrity in acute lung injury.Autophagy · 2018Article
- Autophagy inhibitor 3-methyladenine alleviates overload-exercise-induced cardiac injury in rats.Acta pharmacologica Sinica · 2017Article
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatopulmonary syndrome (HPS) is a defective liver-induced pulmonary vascular disorder with massive pulmonary microvascular dilation and excessive proliferation of pulmonary microvascular endothelial cells (PMVECs). Growing evidence suggests that autophagy is involved in pulmonary diseases, protectively or detrimentally. Thus, it is interesting and important to explore whether autophagy might be involved in and critical in HPS. In the present study, we report that autophagy was activated in common bile duct ligation (CBDL) rats and cultured pulmonary PMVECs induced by CBDL rat serum, two accepted in vivo and in vitro experimental models of HPS. Furthermore, pharmacological inhibition of autophagy with 3-methyladenine (3-MA) significantly alleviated pathological alterations and typical symptom of HPS in CBDL rats in vivo, and consistently 3-MA significantly attenuated the CBDL rat serum-induced excessive proliferation of PMVECs in vitro. All these changes mediated by 3-MA might explain the observed prominent improvement of pulmonary appearance, edema, microvascular dilatation and arterial oxygenation in vivo. Collectively, these results suggest that autophagy activation may play a critical role in the pathogenesis of HPS, and autophagy inhibition may have a therapeutic potential for this disease.
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