ArticleScientific reports2017
Chronic vitamin D deficiency induces lung fibrosis through activation of the renin-angiotensin system.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed, 111 citations in OpenAlex.
- Vitamin D in Cardiovascular Medicine: From Molecular Mechanisms to Clinical Translation.Nutrients · 2026Review
- Low 1,25-dihydroxyvitamin D levels are associated with severe COVID-19: an observational study in hospitalized patients.Frontiers in nutrition · 2026Article
- Paricalcitol Attenuates Bleomycin-induced Pulmonary Fibrosis: Insights from Immunohistochemical and Molecular Genetic Analysis.Endocrine, metabolic & immune disorders drug targets · 2026Article
- Vitamin D exerts endogenous control over TiScience · 2025Article
- Nutritional Support of Chronic Obstructive Pulmonary Disease.Nutrients · 2025Review
- Correlation between orthostatic intolerance in children and levels of ACE2-Ang(1-7)-Mas axis and vitamin D.Frontiers in pediatrics · 2025Article
- A pilot metabolomics study across the continuum of interstitial lung disease fibrosis severity.Physiological reports · 2024Article
- Effects of Immunotoxicity biomarkers, essential elements and vitamin D levels on the severity levels of COVID-19 disease in Turkey.Toxicology research · 2024Article
- Beneficial Impact of Inhaled 25(OH)-Vitamin D3 and 1,25(OH)2-Vitamin D3 on Pulmonary Response in the Murine Model of Hypersensitivity Pneumonitis.International journal of molecular sciences · 2024Article
- Cellular and Molecular Genetic Mechanisms of Lung Fibrosis Development and the Role of Vitamin D: A Review.International journal of molecular sciences · 2024Review
- Association between systemic lupus erythematosus and osteoporosis: a mendelian randomization analysis.BMC rheumatology · 2024Article
- Review
- Fibroblast Upregulation of Vitamin D Receptor Represents a Self-Protective Response to Limit Fibroblast Proliferation and Activation during Pulmonary Fibrosis.Antioxidants (Basel, Switzerland) · 2023Article
- Review
- Correlation of vitamin D levels with serum parameters in Covid-19 patients.Clinical nutrition ESPEN · 2023Article
- First Characterization of the Transcriptome of Lung Fibroblasts of SSc Patients and Healthy Donors of African Ancestry.International journal of molecular sciences · 2023Article
- Metabolomics of VToxicology and applied pharmacology · 2023Article
- The Efficacious Benefit of 25-Hydroxy Vitamin D to Prevent COVID-19: An In-Silico Study Targeting SARS-CoV-2 Spike Protein.Nutrients · 2022Article
- Effects of Vitamin D on the Renin-Angiotensin System and Acute Childhood Pneumonia.Antibiotics (Basel, Switzerland) · 2022Article
- Recent advances in vitamin D implications in chronic respiratory diseases.Respiratory research · 2022Review
4 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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