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2017 ; 7
(1
): 3312
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Chronic vitamin D deficiency induces lung fibrosis through activation of the
renin-angiotensin system
#MMPMID28607392
Shi Y
; Liu T
; Yao L
; Xing Y
; Zhao X
; Fu J
; Xue X
Sci Rep
2017[Jun]; 7
(1
): 3312
PMID28607392
show ga
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.