Chronic vitamin D deficiency induces lung fibrosis through activation of the renin-angiotensin system

Abstract Pulmonary fibrosis, which influences lung function and exacerbates a patient’s condition, is the ultimate stage of many lung diseases. Vitamin D deficiency is associated with pulmonary fibrosis and impaired lung function, but the underlying mechanism has not yet been fully elucidated. Moreo...

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Autores principales:	Yongyan Shi, Tianjing Liu, Li Yao, Yujiao Xing, Xinyi Zhao, Jianhua Fu, Xindong Xue
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/2c9ed688d0fa4b63bdf39a7ffe1aeabc
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spelling	oai:doaj.org-article:2c9ed688d0fa4b63bdf39a7ffe1aeabc2021-12-02T11:52:44ZChronic vitamin D deficiency induces lung fibrosis through activation of the renin-angiotensin system10.1038/s41598-017-03474-62045-2322https://doaj.org/article/2c9ed688d0fa4b63bdf39a7ffe1aeabc2017-06-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-03474-6https://doaj.org/toc/2045-2322Abstract Pulmonary fibrosis, which influences lung function and exacerbates a patient’s condition, is the ultimate stage of many lung diseases. Vitamin D deficiency is associated with pulmonary fibrosis and impaired lung function, but the underlying mechanism has not yet been fully elucidated. Moreover, vitamin D deficiency may cause over-activation of the renin-angiotensin system (RAS), which aggravates extracellular matrix (ECM) deposition and lung fibrosis. This study aims to investigate the effect of chronic vitamin D deficiency on lung fibrosis in otherwise healthy mice and to explore the role of RAS in this process. Mice were depleted of vitamin D through diet control and were compared with healthy subjects. Chronic vitamin D deficiency destructs lung structures, impairs lung development and stimulates ECM deposition. RAS components are also found to increase. These effects seem to worsen with prolonged vitamin D deficiency. By giving RAS blockers, these changes can be largely rescued. However, a smooth muscle relaxant whose regulatory effect on blood pressure is independent of RAS does not show similar effects. This study demonstrated that chronic vitamin D deficiency may induce RAS activation, which subsequently stimulates the expression of profibrotic factors and activates the fibrotic cascade. This profibrotic effect of RAS is independent of elevated blood pressure.Yongyan ShiTianjing LiuLi YaoYujiao XingXinyi ZhaoJianhua FuXindong XueNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-10 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Yongyan Shi Tianjing Liu Li Yao Yujiao Xing Xinyi Zhao Jianhua Fu Xindong Xue Chronic vitamin D deficiency induces lung fibrosis through activation of the renin-angiotensin system
description	Abstract Pulmonary fibrosis, which influences lung function and exacerbates a patient’s condition, is the ultimate stage of many lung diseases. Vitamin D deficiency is associated with pulmonary fibrosis and impaired lung function, but the underlying mechanism has not yet been fully elucidated. Moreover, vitamin D deficiency may cause over-activation of the renin-angiotensin system (RAS), which aggravates extracellular matrix (ECM) deposition and lung fibrosis. This study aims to investigate the effect of chronic vitamin D deficiency on lung fibrosis in otherwise healthy mice and to explore the role of RAS in this process. Mice were depleted of vitamin D through diet control and were compared with healthy subjects. Chronic vitamin D deficiency destructs lung structures, impairs lung development and stimulates ECM deposition. RAS components are also found to increase. These effects seem to worsen with prolonged vitamin D deficiency. By giving RAS blockers, these changes can be largely rescued. However, a smooth muscle relaxant whose regulatory effect on blood pressure is independent of RAS does not show similar effects. This study demonstrated that chronic vitamin D deficiency may induce RAS activation, which subsequently stimulates the expression of profibrotic factors and activates the fibrotic cascade. This profibrotic effect of RAS is independent of elevated blood pressure.
format	article
author	Yongyan Shi Tianjing Liu Li Yao Yujiao Xing Xinyi Zhao Jianhua Fu Xindong Xue
author_facet	Yongyan Shi Tianjing Liu Li Yao Yujiao Xing Xinyi Zhao Jianhua Fu Xindong Xue
author_sort	Yongyan Shi
title	Chronic vitamin D deficiency induces lung fibrosis through activation of the renin-angiotensin system
title_short	Chronic vitamin D deficiency induces lung fibrosis through activation of the renin-angiotensin system
title_full	Chronic vitamin D deficiency induces lung fibrosis through activation of the renin-angiotensin system
title_fullStr	Chronic vitamin D deficiency induces lung fibrosis through activation of the renin-angiotensin system
title_full_unstemmed	Chronic vitamin D deficiency induces lung fibrosis through activation of the renin-angiotensin system
title_sort	chronic vitamin d deficiency induces lung fibrosis through activation of the renin-angiotensin system
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/2c9ed688d0fa4b63bdf39a7ffe1aeabc
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Chronic vitamin D deficiency induces lung fibrosis through activation of the renin-angiotensin system

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