2018
DOI: 10.3892/mmr.2018.8426
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Association between ACE2/ACE balance and pneumocyte apoptosis in a porcine model of acute pulmonary thromboembolism with cardiac arrest

Abstract: Acute pulmonary embolism (APE) is frequently reported in patients with cardiac arrest (CA) in emergency care. Pneumocyte apoptosis is commonly observed in the lungs following an APE. An important pathological mechanism evoking apoptosis during a lipopolysaccharide-induced acute lung injury is the angiotensin-converting enzyme 2 (ACE2)/ACE imbalance. The present study uses a porcine model to examine the anti-apoptotic effects of captopril on APE-CA and the return of spontaneous circulation (ROSC). Pigs were ran… Show more

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Cited by 10 publications
(12 citation statements)
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“…In the respiratory system, angiotensin-converting enzyme 2 expression facilitates the entry of SARS-CoV-2, which mainly infects ciliated cells and type II alveolar cells [ 33 ]. After entry, the SARS-CoV-2 virus causes deregulation of the renin–angiotensin–aldosterone system, displacing the axis in favour of angiotensin II, which can generate lung damage due to activation of the inflammatory cascade [ 34 ], increased type I collagen with consequent decrease in lung compliance [ 35 ] and alveolar cell apoptosis [ 36 ]. In spite of this, approximately 5% of cases evolve to critical conditions [ 37 ], and the presence of comorbidities seems to be decisive.…”
Section: Discussionmentioning
confidence: 99%
“…In the respiratory system, angiotensin-converting enzyme 2 expression facilitates the entry of SARS-CoV-2, which mainly infects ciliated cells and type II alveolar cells [ 33 ]. After entry, the SARS-CoV-2 virus causes deregulation of the renin–angiotensin–aldosterone system, displacing the axis in favour of angiotensin II, which can generate lung damage due to activation of the inflammatory cascade [ 34 ], increased type I collagen with consequent decrease in lung compliance [ 35 ] and alveolar cell apoptosis [ 36 ]. In spite of this, approximately 5% of cases evolve to critical conditions [ 37 ], and the presence of comorbidities seems to be decisive.…”
Section: Discussionmentioning
confidence: 99%
“…But no effect in control rats Abuohashish, Ahmed, Sabry, Khattab, & Al-Rejaie (2017) Captopril/ ACE-Inh. Land race pigs/Pulmonary embolism model No change in pulmonary ACE2 protein expression H. L. Xiao et al (2018) Captopril/ ACE-Inh. Spontaneously hypertensive and Wistar Kyoto rats/ Aortic tissue Markedly decreased aortic ACE2 mRNA expression in hypertensive rats with significantly upregulated ACE2 levels Lezama-Martinez et al (2018) Captopril/ ACE-Inh.…”
Section: Cardiovascular Drugs and Ace2mentioning
confidence: 99%
“…It is also present in the epithelium lining the lung, the nose, and mouth [ 36 ]. It is highly abundant in type 2 pneumocytes, the important cells located in alveoli, where oxygen exchanged with carbon dioxide [ 37 ]. Regulating blood pressure and inflammation are the main functions of local ACE2 via the conversion of angiotensin II (Ang II) to other molecules that neutralize the effects of Ang II.…”
Section: Introductionmentioning
confidence: 99%