4.2 Review

Association of the ACE2-Angiotensin1-7-Mas axis with lung damage caused by cigarette smoke exposure: a systematic review

Journal

REVIEWS ON ENVIRONMENTAL HEALTH
Volume -, Issue -, Pages -

Publisher

WALTER DE GRUYTER GMBH
DOI: 10.1515/reveh-2023-0028

Keywords

ACE2; Angiotensin1-7; cigarette smoke; lung damage; Mas receptor

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This systematic review aimed to explore the relationship between lung damage caused by cigarette smoke exposure and the ACE2-Ang-(1-7)-Mas pathway. The majority of studies concluded that cigarette smoke exposure increases the risk of lung damage, supporting the involvement of the renin-angiotensin system in smoking-induced damage. The protective ACE2-Ang-(1-7)-Mas pathway has been shown to significantly influence the etiology of lung inflammation.
Through the Mas receptor, angiotensin-(1-7) [Ang-(1-7)] has been shown to have a key role in the development of lung inflammation. This systematic review (SR) sought to identify the relationship between lung damage brought on by exposure to cigarette smoke (CS) and the ACE2-Ang-(1-7)-Mas pathway. In this investigation, relevant keywords were used to search PubMed (MEDLINE), Scopus (Elsevier), and Institute for Scientific Information (ISI) Web of Science up to December 2022. Nine studies were chosen because they satisfied the inclusion/exclusion criteria. The majority of research concluded that exposure to CS increased the risk of lung damage. Smoking cigarettes is the main cause of COPD because it causes massive amounts of reactive oxygen and nitrogen species to enter the lungs, which stimulate the production of inflammatory cytokines like IL-1 beta, IL-6, and TNF-alpha, as well as the invasion of inflammatory cells like neutrophils and macrophages. These findings support the renin-angiotensin system's (RAS) involvement in the pathophysiology of smoking-induced damage. Additionally, via stimulating pro-inflammatory mediators, aberrant RAS activity has been linked to lung damage. Lung inflammation's etiology has been shown to be significantly influenced by the protective known RAS arm ACE2-Ang-(1-7)-Mas. In conclusion, these are important for informing policymakers to pass legislation limiting the use of smoking and other tobacco to prevent their harmful effects.

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