ArticleJournal of the renin-angiotensin-aldosterone system : JRAAS2015
Activation of renin-angiotensin-aldosterone system (RAAS) in the lung of smoking-induced pulmonary arterial hypertension (PAH) rats.
Article in Journal of the renin-angiotensin-aldosterone system : JRAAS, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 2 of them syntheses that pooled it.
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Who cites it
48 citing papers in PubMed, 2 syntheses or guidelines pooled it, 77 citations in OpenAlex.
- Association of the ACE2-Angiotensin1-7-Mas axis with lung damage caused by cigarette smoke exposure: a systematic review.Reviews on environmental health · 2024Pooled it
- Overexpression of angiotensin-converting enzyme 2 by renin-angiotensin system inhibitors. Truth or myth? A systematic review of animal studies.Hypertension research : official journal of the Japanese Society of Hypertension · 2021Pooled it
- Fenofibrate as a Modulator of the Renin-Angiotensin System in Su/Hx-Induced Pulmonary Arterial Hypertension.International journal of molecular sciences · 2025Article
- Nicotinism vs. Glomerulopathies-Smoking as a Risk Factor for Primary Glomerulopathies.Antioxidants (Basel, Switzerland) · 2025Review
- The renin-angiotensin system in models of pulmonary arterial hypertension vs primary hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2025Review
- Review
- Aging and "Age-Related" Diseases - What Is the Relation?Aging and disease · 2024Review
- Angiotensin-Converting Enzyme 2 (ACE2) Signaling in Pulmonary Arterial Hypertension: Underpinning Mechanisms and Potential Targeting Strategies.International journal of molecular sciences · 2023Article
- ACE2 overexpression in corticotropin-releasing-hormone cells offers protection against pulmonary hypertension.Frontiers in neuroscience · 2023Article
- When the clock ticks wrong with COVID-19.Clinical and translational medicine · 2022Review
- Ovarian hormones do not mediate protection against pulmonary hypertension and right ventricular remodeling in female mice exposed to chronic, inhaled nicotine.American journal of physiology. Heart and circulatory physiology · 2022Article
- Renin-angiotensin system blockade on angiotensin-converting enzyme 2 and TMPRSS2 in human type II pneumocytes.Life sciences · 2022Observational
- Pathogenesis of (smoking-related) non-communicable diseases-Evidence for a common underlying pathophysiological pattern.Frontiers in physiology · 2022Review
- Review
- A 2-month post-COVID-19 follow-up study on patients with dyspnea.Health science reports · 2021Article
- Active site-specific quantum tunneling of hACE2 receptor to assess its complexing poses with selective bioactive compounds in co-suppressing SARS-CoV-2 influx and subsequent cardiac injury.Journal of advanced veterinary and animal research · 2021Article
- Alternative RAS in Various Hypoxic Conditions: From Myocardial Infarction to COVID-19.International journal of molecular sciences · 2021Review
- Renin Angiotensin Aldosterone System Antagonism in 2019 Novel Coronavirus Acute Lung Injury.Open forum infectious diseases · 2021Review
- Review
- Critical Determinants of Cytokine Storm and Type I Interferon Response in COVID-19 Pathogenesis.Clinical microbiology reviews · 2021Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesTo explore the role of the renin-angiotensin-aldosterone system (RAAS) in the pathogenesis of pulmonary arterial hypertension (PAH) induced by chronic exposure to cigarette smoke.
methods48 healthy male SD rats were randomly divided into four groups (12/group): control group (group A); inhibitor alone group (group B); cigarette induction group (group C); cigarette induction + inhibitor group (group D). After the establishment of smoking-induced PAH rat model, the right ventricular systolic pressure (RVSP) was detected using an inserted catheter; western blotting was used to detect the protein expression of angiotensin-converting enzyme-2 (ACE2) and angiotensin-converting enzyme (ACE); expression levels of angiotensin II (AngII) in lung tissue were measured by radioimmunoassay.
resultsAfter six months of cigarette exposure, the RVSP of chronic cigarette induction group was significantly higher than that of the control group; expression levels of AngII and ACE increased in lung tissues, but ACE2 expression levels reduced. Compared with cigarette exposure group, after losartan treatment, RVSP, ACE and AngII obviously decreased (P<0.05), and ACE2 expression levels significantly increased.
conclusionChronic cigarette exposure may result in PAH and affect the protein expression of ACE2 and ACE in lung tissue, suggesting that ACE2 and ACE play an important role in the pathogenesis of smoking-induced PAH.
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