Ginkgolide B Blocks Vascular Remodeling after Vascular Injury via Regulating Tgfβ1/Smad Signaling Pathway
Coronary artery disease (CAD) is the most prevalent cardiovascular disease worldwide, resulting in myocardial infarction (MI) and even sudden death. Following percutaneous coronary intervention (PCI), restenosis caused by vascular remodeling is always formed at the stent implantation site. Here, we...
| Main Authors: | , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Hindawi-Wiley
2023-01-01
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| Series: | Cardiovascular Therapeutics |
| Online Access: | http://dx.doi.org/10.1155/2023/8848808 |
| _version_ | 1797384435296894976 |
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| author | Quan Wang Shuai Ni Li Ling Siqi Wang Hanbin Xie Zhanhong Ren |
| author_facet | Quan Wang Shuai Ni Li Ling Siqi Wang Hanbin Xie Zhanhong Ren |
| author_sort | Quan Wang |
| collection | DOAJ |
| description | Coronary artery disease (CAD) is the most prevalent cardiovascular disease worldwide, resulting in myocardial infarction (MI) and even sudden death. Following percutaneous coronary intervention (PCI), restenosis caused by vascular remodeling is always formed at the stent implantation site. Here, we show that Ginkgolide B (GB), a naturally occurring terpene lactone, effectively suppresses vascular remodeling and subsequent restenosis in wild-type mice following left carotid artery (LCA) injury. Additional experiments reveal that GB exerts a protective effect on vascular remodeling and further restenosis through modulation of the Tgfβ1/Smad signaling pathway in vivo and in human vascular smooth muscle cells (HVSMAs) but not in human umbilical vein endothelial cells (HUVECs) in vitro. Moreover, the beneficial effect of GB is abolished after incubated with pirfenidone (PFD, a drug for idiopathic pulmonary fibrosis, IPF), which can inhibit Tgfβ1. In Tgfβ1-/- mice, treatment with pirfenidone capsules and Yinxingneizhi Zhusheye (including Ginkgolide B) fails to improve vascular remodeling and restenosis. In conclusion, our data identify that GB could be a potential novel therapeutic agent to block vessel injury-associated vascular remodeling and further restenosis and show significant repression of Tgfβ1/Smad signaling pathway. |
| first_indexed | 2024-03-08T21:35:32Z |
| format | Article |
| id | doaj.art-c157375fea6c4b6b978317f3649e8d91 |
| institution | Directory Open Access Journal |
| issn | 1755-5922 |
| language | English |
| last_indexed | 2024-03-08T21:35:32Z |
| publishDate | 2023-01-01 |
| publisher | Hindawi-Wiley |
| record_format | Article |
| series | Cardiovascular Therapeutics |
| spelling | doaj.art-c157375fea6c4b6b978317f3649e8d912023-12-21T00:00:46ZengHindawi-WileyCardiovascular Therapeutics1755-59222023-01-01202310.1155/2023/8848808Ginkgolide B Blocks Vascular Remodeling after Vascular Injury via Regulating Tgfβ1/Smad Signaling PathwayQuan Wang0Shuai Ni1Li Ling2Siqi Wang3Hanbin Xie4Zhanhong Ren5Hubei University of Science and TechnologyGerman Cancer Research Center (DKFZ)School of PharmacyHubei University of Science and TechnologyCollections Conservation Research CenterHubei University of Science and TechnologyCoronary artery disease (CAD) is the most prevalent cardiovascular disease worldwide, resulting in myocardial infarction (MI) and even sudden death. Following percutaneous coronary intervention (PCI), restenosis caused by vascular remodeling is always formed at the stent implantation site. Here, we show that Ginkgolide B (GB), a naturally occurring terpene lactone, effectively suppresses vascular remodeling and subsequent restenosis in wild-type mice following left carotid artery (LCA) injury. Additional experiments reveal that GB exerts a protective effect on vascular remodeling and further restenosis through modulation of the Tgfβ1/Smad signaling pathway in vivo and in human vascular smooth muscle cells (HVSMAs) but not in human umbilical vein endothelial cells (HUVECs) in vitro. Moreover, the beneficial effect of GB is abolished after incubated with pirfenidone (PFD, a drug for idiopathic pulmonary fibrosis, IPF), which can inhibit Tgfβ1. In Tgfβ1-/- mice, treatment with pirfenidone capsules and Yinxingneizhi Zhusheye (including Ginkgolide B) fails to improve vascular remodeling and restenosis. In conclusion, our data identify that GB could be a potential novel therapeutic agent to block vessel injury-associated vascular remodeling and further restenosis and show significant repression of Tgfβ1/Smad signaling pathway.http://dx.doi.org/10.1155/2023/8848808 |
| spellingShingle | Quan Wang Shuai Ni Li Ling Siqi Wang Hanbin Xie Zhanhong Ren Ginkgolide B Blocks Vascular Remodeling after Vascular Injury via Regulating Tgfβ1/Smad Signaling Pathway Cardiovascular Therapeutics |
| title | Ginkgolide B Blocks Vascular Remodeling after Vascular Injury via Regulating Tgfβ1/Smad Signaling Pathway |
| title_full | Ginkgolide B Blocks Vascular Remodeling after Vascular Injury via Regulating Tgfβ1/Smad Signaling Pathway |
| title_fullStr | Ginkgolide B Blocks Vascular Remodeling after Vascular Injury via Regulating Tgfβ1/Smad Signaling Pathway |
| title_full_unstemmed | Ginkgolide B Blocks Vascular Remodeling after Vascular Injury via Regulating Tgfβ1/Smad Signaling Pathway |
| title_short | Ginkgolide B Blocks Vascular Remodeling after Vascular Injury via Regulating Tgfβ1/Smad Signaling Pathway |
| title_sort | ginkgolide b blocks vascular remodeling after vascular injury via regulating tgfβ1 smad signaling pathway |
| url | http://dx.doi.org/10.1155/2023/8848808 |
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