Basigin Mediates Pulmonary Hypertension by Promoting Inflammation and Vascular Smooth Muscle Cell Proliferation

Satoh, Kimio; Satoh, Taijyu; Kikuchi, Nobuhiro; Omura, Junichi; Kurosawa, Ryo; Suzuki, Kota; Sugimura, Koichiro; Aoki, Tatsuo; Nochioka, Kotaro; Tatebe, Shunsuke; Miyamichi-Yamamoto, Saori; Miura, Masanobu; Shimizu, Tôru; Ikeda, Shohei; Yaoita, Nobuhiro; Fukumoto, Yoshihiro; Minami, Tatsuro; Miyata, Satoshi; Nakamura, Kazufumi; Ito, Hiroshi; Kadomatsu, Kenji; Shimokawa, Hiroaki

doi:10.1161/circresaha.115.304563

Cited by 90 publications

(110 citation statements)

References 66 publications

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“…17,18 The pathobiology of PAH includes EC dysfunction, VSMC proliferation/migration, and inflammation. [19][20][21][22][23] PDGF has been implicated in these processes 24 and altered PDGF signaling is involved in the vascular remodeling observed in PAH. 22 Thus, PDE1C may represent a novel therapeutic target for VSMC phenotypic modulation in systemic hypertension, aneurysms, and PAH.…”

Section: Clinical Perspectivesmentioning

confidence: 99%

PDE1C Negatively Regulates Growth Factor Receptor Degradation and Promotes VSMC Proliferation

Satoh

Kikuchi

Kurosawa

et al. 2015

Circulation Research

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Section: Clinical Perspectivesmentioning

confidence: 99%

PDE1C Negatively Regulates Growth Factor Receptor Degradation and Promotes VSMC Proliferation

Satoh

Kikuchi

Kurosawa

et al. 2015

Circulation Research

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“…18 As expected, extracellular CyPA and vascular Bsg played a crucial role in hypoxia-induced PH by inducing growth factor secretion, inflammatory cell recruitment, and VSMC proliferation. 30 Moreover, extracellular CyPA induced secretion of cytokines/chemokines and growth factors from PAH-PASMCs, and this effect was enhanced by hypoxia. In a clinical study, plasma CyPA levels were increased and predicted poor outcomes in patients with PAH.…”

Section: Conclusion and Future Perspectivesmentioning

confidence: 98%

“…17 In a series of studies, it has been found that intracellular and extracellular CyPA promote intimal thickening, 24 abdominal aortic aneurysms (AAA), 26 atherosclerosis, 28 cardiac hypertrophy, 29 and PH. 30 Based on these results, translational research on patients with coronary artery disease (CAD) examined the prognostic importance of CyPA, followed by a series of clinical studies. 8,16,30,31,33, 39 Plasma levels of CyPA were significantly increased in patients with angiographically proven CAD.…”

Section: Abdominal Aortic Aneurysmsmentioning

confidence: 99%

“…Recently, it was demonstrated that Bsg is a receptor for VSMCs. 30 It is expressed in cardiac fibroblasts, secreted by mechanical stretch, and activates MMPs in cardiac tissues. 45 Importantly, Bsg disrupts NO metabolism and causes harmful endothelial activation, including Rho-kinase activation.…”

Section: Abdominal Aortic Aneurysmsmentioning

confidence: 99%

“…In a clinical study, plasma CyPA levels were increased and predicted poor outcomes in patients with PAH. 30 In addition to CyPA and Bsg, several novel pathogenic proteins that are potentially useful biomarkers for PAH have been found. 59-61 imaging techniques to evaluate pulmonary arterial remodeling in patients with PAH have been developed, 62, 63 and, in addition, it has been found that pravastatin and metformin ameliorate hypoxia-induced PH in mice.…”

Section: Conclusion and Future Perspectivesmentioning

confidence: 99%

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Development of Novel Therapies for Cardiovascular Diseases by Clinical Application of Basic Research

Satoh

2017

Circ J

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Cyclophilin A (CyPA) is secreted from vascular smooth muscle cells, inflammatory cells, activated platelets, and cardiac fibroblasts in response to oxidative stress. Excessive and continuous activation of the RhoA/Rho-kinase system promotes the secretion of CyPA, resulting in the development of multiple cardiovascular diseases. Basigin (Bsg), a transmembrane glycoprotein that activates matrix metalloproteinases, is an extracellular receptor for CyPA that promotes cell proliferation and inflammation. Thus, the CyPA/Bsg system is potentially a novel therapeutic target for cardiovascular diseases. Importantly, plasma CyPA levels are increased in patients with coronary artery disease, abdominal aortic aneurysms, pulmonary hypertension, and heart failure. Moreover, plasma CyPA levels can predict all-cause death in patients with coronary artery disease and pulmonary hypertension. Additionally, plasma soluble Bsg levels are increased and predict all-cause death in patients with heart failure, suggesting that CyPA and Bsg are novel biomarkers for cardiovascular diseases. To discover further novel molecules targeting the CyPA/Bsg system, high-throughput screening of compounds found molecules that ameliorate the development of cardiovascular diseases. In addition to CyPA and Bsg, novel therapeutic targets and their inhibitors for patients with pulmonary arterial hypertension have been recently screened and identified. Ultimately, the final goal is to develop novel biomarkers and medications that will be useful for improving the prognosis and quality of life in patients with cardiovascular diseases.

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Adverse effects of ambient fine particulate matter (PM_2.5) on vascular smooth muscle cells

Ming

Liu

et al. 2022

J of Applied Toxicology

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Cardiovascular diseases are the leading cause of death worldwide. Meanwhile, environment air pollution has become a serious health risk factor, contributing to the mortality of respiratory and cardiovascular diseases. A substantial body of evidence has shown that many types of vascular diseases are related to air pollution. The physiology and pathophysiology of the three layers of vascular vessels, especially the inner and medial layer, contribute to the process of vascular diseases. Vascular smooth muscle cells (VSMCs) are the predominant cells in the medial layer, and several studies have indicated that air pollution has an adverse effect on VSMCs. There are numerous sources of air pollution across the world, and the components of air pollutants are a complex mixture of gaseous pollutants and particulate matter. Among these air pollutants, particulate matter (PM)2.5 presents the highest risk factor leading to global mortality from cardiovascular disease and disability. In this review, we primarily focus on the impacts of PM2.5 exposure on VSMCs. We further discuss the correlation between exposure to PM2.5 and other vascular diseases and present potential protective and treatment strategies to decrease vascular mortality related to air pollution.

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Basigin Mediates Pulmonary Hypertension by Promoting Inflammation and Vascular Smooth Muscle Cell Proliferation

Cited by 90 publications

References 66 publications

PDE1C Negatively Regulates Growth Factor Receptor Degradation and Promotes VSMC Proliferation

PDE1C Negatively Regulates Growth Factor Receptor Degradation and Promotes VSMC Proliferation

Development of Novel Therapies for Cardiovascular Diseases by Clinical Application of Basic Research

Adverse effects of ambient fine particulate matter (PM_2.5) on vascular smooth muscle cells

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Basigin Mediates Pulmonary Hypertension by Promoting Inflammation and Vascular Smooth Muscle Cell Proliferation

Cited by 90 publications

References 66 publications

PDE1C Negatively Regulates Growth Factor Receptor Degradation and Promotes VSMC Proliferation

PDE1C Negatively Regulates Growth Factor Receptor Degradation and Promotes VSMC Proliferation

Development of Novel Therapies for Cardiovascular Diseases by Clinical Application of Basic Research

Adverse effects of ambient fine particulate matter (PM2.5) on vascular smooth muscle cells

Contact Info

Product

Resources

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Adverse effects of ambient fine particulate matter (PM_2.5) on vascular smooth muscle cells