Abstract
Vitamin A (all-trans-retinol) is a fat-soluble micronutrient which together with its natural derivatives and synthetic analogues constitutes the group of retinoids. They are involved in a wide range of physiological processes such as embryonic development, vision, immunity and cellular differentiation and proliferation. Retinoic acid (RA) is the main active form of vitamin A and multiple genes respond to RA signalling through transcriptional and non-transcriptional mechanisms. Vitamin A deficiency (VAD) is a remarkable public health problem. An adequate vitamin A intake is required in early lung development, alveolar formation, tissue maintenance and regeneration. In fact, chronic VAD has been associated with histopathological changes in the pulmonary epithelial lining that disrupt the normal lung physiology predisposing to severe tissue dysfunction and respiratory diseases. In addition, there are important alterations of the structure and composition of extracellular matrix with thickening of the alveolar basement membrane and ectopic deposition of collagen I. In this review, we show our recent findings on the modification of cell-junction proteins in VAD lungs, summarize up-to-date information related to the effects of chronic VAD in the impairment of lung physiology and pulmonary disease which represent a major global health problem and provide an overview of possible pathways involved.
Highlights
Vitamin A is a fat-soluble micronutrient which, together with its natural derivatives and synthetic analogues that exhibit its biological activity, constitutes the group of retinoids [1]
We have reported that collagens I and IV show an increase in the lungs of Vitamin A deficiency (VAD) rats and, in parallel, the alveolar basement membrane (BM) doubles in thickness and appears to have an ectopic deposition of collagen I fibrils inside
In a model of chronic VAD rats we have shown that vitamin deficiency during the growing period results in emphysemic lungs, which associates with alterations in extracellular matrix (ECM)/BM and an increase in transforming growth factor β (TGF-β) levels in pulmonary tissue
Summary
Vitamin A (all-trans-retinol) is a fat-soluble micronutrient which, together with its natural derivatives and synthetic analogues that exhibit its biological activity, constitutes the group of retinoids [1]. Vitamin A is involved in the proliferation and maintenance of epithelial cells, including those of the respiratory tract It is a major factor regulating differentiation and maturation of the lung, and maternal. VAD has been associated with histopathological changes in the pulmonary epithelial lining and in lung parenchyma which leads to disrupt the normal lung physiology and predisposes to severe tissue dysfunction and respiratory diseases These alterations are associated with changes in the extracellular matrix (ECM) and basement membrane (BM) protein content and distribution [30,31,32]. We report our recent findings on the modification of cell-junction proteins in VAD lungs and summarize the information available on the effects of chronic VAD in the impairment of lung physiology and pulmonary disease, which represent a major global health problem [35] and provide an overview of the possible pathways involved
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