Mangiferin alleviates diabetic pulmonary fibrosis in mice via inhibiting endothelial-mesenchymal transition through AMPK/FoxO3/SIRT3 axis
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Diabetes mellitus results in numerous complications. Diabetic pulmonary fibrosis (DPF), a late pulmonary complication of diabetes, has not attracted as much attention as diabetic nephropathy and cardiomyopathy. Mangiferin (MF) is a natural small molecular compound that exhibits a variety of pharmacological effects including anti-inflammatory, anti-cancer, anti-diabetes, and anti-fibrosis effects. In this study, we investigated whether long-term diabetes shock induces DPF, and explored whether MF had a protective effect against DPF. We first examined the lung tissues and sections of 20 diabetic patients obtained from discarded lung surgical resection specimens and found that pulmonary fibrosis mainly accumulated around the pulmonary vessels, accompanied by significantly enhanced endothelial-mesenchymal transition (EndMT). We established a mouse model of DPF by STZ injections. Ten days after the final STZ injection, the mice were administered MF (20, 60 mg/kg, i.g.) every 3 days for 4 weeks, and kept feeding until 16 weeks and euthanized. We showed that pulmonary fibrotic lesions were developed in the diabetic mice, which began around the pulmonary vessels, while MF administration did not affect long-term blood glucose levels, but dose-dependently alleviated diabetes-induced pulmonary fibrosis. In human umbilical vein endothelial cells (HUVECs), exposure to high glucose (33.3 mM) induced EndMT, which was dose-dependently inhibited by treatment with MF (10, 50 μM). Furthermore, MF treatment promoted SIRT3 expression in high glucose-exposed HUVECs by directly binding to AMPK to enhance the activity of FoxO3, which finally reversed diabetes-induced EndMT. We conclude that MF attenuates DPF by inhibiting EndMT through the AMPK/FoxO3/SIRT3 axis. MF could be a potential candidate for the early prevention and treatment of DPF.
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In diabetic pulmonary fibrosis, MGF inhibits endothelial-mesenchymal transition and modulates the AMPK/FoxO3/SIRT3 pathway, as evidenced by changes in pathway proteins and fibrosis markers.
“Reported effects include the inhibition of endothelial-mesenchymal transition and modulation of the AMPK/FoxO3/sirtuin (SIRT)3 pathway, as evidenced by changes in pathway proteins and fibrosis markers (33).”
From Mangiferin in human disease: Multifaceted mechanisms and applications (Review) (2026) · cites this paper as [33]
In a mouse model of diabetic pulmonary fibrosis, oral administration of 60 mg/kg MGF every 3 days for 4 weeks reduces the progression of fibrosis.
“In a mouse model of diabetic pulmonary fibrosis, oral administration of 60 mg/kg MGF every 3 days for 4 weeks has been shown to reduce the progression of fibrosis.”
From Mangiferin in human disease: Multifaceted mechanisms and applications (Review) (2026) · cites this paper as [33]
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Flagged first, then by citations
Research works printed but not linked: 1
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Self-citation
- Authors
- Fu, T.-L., Li, G.-R., Li, D.-H., He, R.-Y., Liu, B.-H., Xiong, R., Xu, C.-Z., Lu, Z.-L., Song, C.-K., Qiu, H.-L., Wang, W.-J., Zou, S.-S., Yi, K., Li, N., & Geng, Q.
- Affiliations
- Renmin Hospital of Wuhan University (CN)
- Corresponding author
- Li, Ning
- Geng, Qing
- Venue
- Acta Pharmacologica Sinica
- Published
- 2024-01-15
- Volume
- 45
- Issue
- 5
- Pages
- 1002-1018
- ISSN
- 0253-9756 (ISSN-L)
- 1671-4083
- 1745-7254
- PMC
- PMC11053064
- OpenAlex
- W4390885427
- Cited by
- 27
- References
- 87
- Citations by year
- 2026: 11 · 2025: 12 · 2024: 4
- FWCI
- 13.50
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- Locations
- Acta Pharmacologica Sinica (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (82102269)
- Fundamental Research Funds for the Central Universities (2042023kf0011)
- Topics
- Health Sciences › Medicine › Complementary and alternative medicine › Mangiferin and Mango Extracts
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
- Health Sciences › Medicine › Nephrology › Chronic Kidney Disease and Diabetes
- Keywords
- mangiferin, endothelial-to-mesenchymal transition, AMPK, FOXO3, SIRT3, high glucose, streptozotocin-induced diabetes, diabetic vascular complications, antifibrotic therapy
- MeSH terms
- Forkhead Box Protein O3, Endothelial-Mesenchymal Transition, Animals, Diabetes Mellitus, Experimental, Humans, Male, Mice, Inbred C57BL, Pulmonary Fibrosis, Streptozocin, Signal Transduction, Xanthones, Mice, AMP-Activated Protein Kinases, Sirtuin 3, Epithelial-Mesenchymal Transition, Human Umbilical Vein Endothelial Cells
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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