About: Impact of Angiotensin II type 1 and G-Protein-Coupled Mas receptor expression on the pulmonary performance of patients with idiopathic pulmonary fibrosis

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About: Impact of Angiotensin II type 1 and G-Protein-Coupled Mas receptor expression on the pulmonary performance of patients with idiopathic pulmonary fibrosis Goto Sponge NotDistinct Permalink

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Impact of Angiotensin II type 1 and G-Protein-Coupled Mas receptor expression on the pulmonary performance of patients with idiopathic pulmonary fibrosis
Creator	Antunes, Helen Fabíola, Adélia Fernandes, Renata Perin, Fabíola Perin, Katya Raupp, Débora Rigatto, Rigatto, Katya
Source	Elsevier; Medline; PMC
abstract	Idiopathic pulmonary fibrosis (IPF) is a severe interstitial disease with a mean survival of about 2.5–5 years after diagnosis. Its pathophysiology is still a major challenge for science. It is known that angiotensin II (Ang-II) binds AT1 receptor (AT1R) and its overactivation induces fibrosis, inflammation and oxidative stress. In contrast, activation of the Mas receptor (Mas-R) by angiotensin 1–7 opposes the harmful effects induced by Ang-II. Thus, our innovative objective was to analyze, in patients’ lung with IPF, the balance between AT1R and Mas-R expression and their possible association with pulmonary spirometric parameters: forced expiratory volume in the first second (FEV(1)%) and forced vital capacity (FVC%). One cubic centimeter of lung tissue was obtained from IPF patients (n = 6) and from patients without IPF (n = 6) who underwent bronchial carcinoma resection. Receptor expression was quantified using western blot. AT1R expression was significantly higher (34%) in patients with IPF (P = 0.006), whereas Mas-R was significantly less expressed (54%) in these patients’ lungs (P = 0.046). There was also a positive correlation between Mas-R expression and FEV(1)% (r = 0.62, P = 0.03) and FVC% (r = 0.58, P = 0.05). Conversely, AT1R expression was negatively correlated with FEV(1)% (r = 0.80, P = 0.002) and FVC% (r = 0.74, P = 0.006). In conclusion, our results demonstrated an increased expression of AT1R and reduced expression of Mas-R in the lung of patients with IPF. The dominance of AT1R expression is associated with reduced lung function, highlighting the role of the renin–angiotensin system peptides in the pathophysiology of IPF.
has issue date	2020-08-07(xsd:dateTime)
bibo:doi	10.1016/j.peptides.2020.170384
bibo:pmid	32777324
has license	no-cc
sha1sum (hex)	70d567c46e43292bd0880eca81df1b0c39cfb870
schema:url	https://doi.org/10.1016/j.peptides.2020.170384
resource representing a document's title	Impact of Angiotensin II type 1 and G-Protein-Coupled Mas receptor expression on the pulmonary performance of patients with idiopathic pulmonary fibrosis
has PubMed Central identifier	PMC7411382
has PubMed identifier	32777324
schema:publication	Peptides
resource representing a document's body	covid:70d567c46e43292bd0880eca81df1b0c39cfb870#body_text
is schema:about of	named entity 'Peptides' named entity 'fibroblasts' named entity 'AT1R' named entity 'lung transplantation' named entity 'messenger RNA' named entity 'IPF' named entity 'SPSS' named entity 'Ang-II' named entity 'AT1R' named entity 'protein kinase' named entity 'Germany' named entity 'BMI' named entity 'ACE' named entity 'Ang-II' named entity 'hypertrophy' named entity 'fibrosis' named entity 'IPF' named entity 'interstitial pneumonia' named entity 'pregnancy' named entity 'Idiopathic pulmonary fibrosis' named entity 'alveolar epithelial cells' named entity 'IPF' named entity 'IPF' named entity 'ACE2' named entity 'lung tissue' named entity 'prognosis' named entity 'positive correlation' named entity 'COVID-19' named entity 'physiological' named entity 'IPF' named entity 'IPF' named entity 'lung tissue' named entity 'IPF' named entity 'AT1R' named entity 'perfect pairing' named entity 'etiology' named entity 'FEV1%' named entity 'negatively correlated' named entity 'Pregnancy' named entity 'antifibrotic' named entity 'Ang-II' named entity 'quality of life' named entity 'fibroblast' named entity 'RAS' named entity 'pulmonary fibrosis' named entity 'forced vital capacity' named entity 'receptor' named entity 'Ang-II' named entity 'alveolar cells' named entity 'peptides' named entity 'IPF' named entity 'blood volume' named entity 'IPF' named entity 'protein' named entity 'standard deviations' named entity 'ACE' named entity 'control group' named entity 'FEV1%' named entity 'resection' named entity 'GE Healthcare' named entity 'IPF' named entity 'IPF' named entity 'IPF' named entity 'human lung' named entity 'cell types' named entity 'lungs' named entity 'RAS' named entity 'forced vital capacity' named entity 'monoclonal antibody' named entity 'bleomycin' named entity 'IPF' named entity 'angiotensin II' named entity 'AT1R' named entity 'normality test'

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