5.2 Monitoring Airway Disease 2015
DOI: 10.1183/13993003.congress-2015.pa3970
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Serum levels of RAAS components in COPD

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Cited by 9 publications
(9 citation statements)
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“…Alterations in local/systemic inflammatory response, impaired host immunity, microbiome imbalance, persistent mucus production, structural damage, and use of inhaled corticosteroids have been hypothesized to contribute to such risk [3]. With respect to COVID-19, levels of angiotensin converting enzyme 2 (ACE2), the reported host receptor of the virus responsible of COVID-19 (severe acute respiratory syndrome coronavirus 2; SARS-CoV-2), have been observed to be increased in patients with COPD [4,5]. However, early individual COVID-19 studies have not consistently reported a significantly higher rate of severe disease in COPD patients [6,7].…”
mentioning
confidence: 99%
“…Alterations in local/systemic inflammatory response, impaired host immunity, microbiome imbalance, persistent mucus production, structural damage, and use of inhaled corticosteroids have been hypothesized to contribute to such risk [3]. With respect to COVID-19, levels of angiotensin converting enzyme 2 (ACE2), the reported host receptor of the virus responsible of COVID-19 (severe acute respiratory syndrome coronavirus 2; SARS-CoV-2), have been observed to be increased in patients with COPD [4,5]. However, early individual COVID-19 studies have not consistently reported a significantly higher rate of severe disease in COPD patients [6,7].…”
mentioning
confidence: 99%
“…The exact mechanism through which COPD makes people more vulnerable to getting COVID-19 or developing a more severe disease was not completely understood [ 98 ]; nonetheless, ACE2 expression was enhanced in the lower respiratory tract of the COPD patients and smokers [ 99 ]. Also, the impaired renin-angiotensin-aldosterone system caused acute pulmonary hypertension and edema [ 98 , 100 ]. Thus, these possible reasons make patients with COPD vulnerable to SARS-CoV-2 infection.…”
Section: Resultsmentioning
confidence: 99%
“…Significant inverse relationships between ACE2 gene expression and predicted forced expiratory volume for 1 s ( r = −[0.24 – 0.40]; P < 0.05) were reported ( 127 , 129 ), and higher ACE2 mRNA and protein levels in lung tissue were seen in moderate to severe COPD ( 128 ). Toru et al ( 135 ) discovered significant serum ACE2 level increases in 27 COPD patients. However, reductions in endothelin-1, which downregulate ACE2, were found during exacerbations of COPD, suggesting that ACE2 dysregulation exacerbates disease potentiation ( 136 , 137 ).…”
Section: Primary Risk Factorsmentioning
confidence: 99%