Angiotensin-converting enzyme 2 in lung diseases

Kuba, Keiji; Imai, Yumiko; Penninger, Josef

doi:10.1016/j.coph.2006.03.001

Cited by 375 publications

(377 citation statements)

References 61 publications

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“…18,19 Angiotensin II generated by ACE promotes lung injury and conversion of fibroblasts into myofibroblasts followed by the accumulation of collagen. 28,29 Epithelioid cells in lung granulomas of ApoE Ϫ/Ϫ mice have shown strong ACE immunoreactivity that, similar to human granulomas, may contribute to the development of fibrotic changes in lungs.…”

Section: Discussionmentioning

confidence: 99%

ApoE-Deficient Mice on Cholate-Containing High-Fat Diet Reveal a Pathology Similar to Lung Sarcoidosis

Samokhin

Bühling

Theissig

et al. 2010

The American Journal of Pathology

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Sarcoidosis is a chronic disease of unknown etiology characterized by the formation of non-necrotizing epithelioid granulomas in various organs , especially in the lungs. The lack of an adequate animal model reflecting the pathogenesis of the human disease is one of the major impediments in studying sarcoidosis. In this report , we describe ApoE ؊/؊ mice on a cholatecontaining high-fat diet that exhibit granulomatous lung inflammation similar to human sarcoidosis. Histological analysis revealed well-defined and non-necrotizing granulomas in about 40% of mice with the highest number of granulomas after 16 weeks on a cholate-containing high-fat diet. Granulomas contained CD4؉ and CD8 ؉ T cells , and the majority of the cells in granulomas showed immunoreactivity for the macrophage marker Mac-3. Cells with morphological features of epithelioid cells expressed angiotensinconverting enzyme , osteopontin , and cathepsin K, all characteristics of epithelioid and giant cells in granulomas of human sarcoidosis. Giant cells and nonspecific inclusions such as Schaumann's bodies and crystalline deposits were also detected in some lungs. Granulomatous inflammation resulted in progressive pulmonary fibrosis. Removal of cholate from the diet prevented the formation of lung granulomas. The observed similarities between the analyzed mouse lung granulomas and granulomas of human sarcoidosis , as well as the chronic disease character leading to fibrosis , suggest that this mouse model might be a useful tool to study sarcoidosis.

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Section: Discussionmentioning

confidence: 99%

ApoE-Deficient Mice on Cholate-Containing High-Fat Diet Reveal a Pathology Similar to Lung Sarcoidosis

Samokhin

Bühling

Theissig

et al. 2010

The American Journal of Pathology

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“…Alterations in the level of AngII can be seen up to the expression level of ACE2 (20). It is thought that the activation of the ACE2 pathway also provides protection against several lung diseases besides the inhibition of the ACE pathway (3). To the best of our knowledge, ACE2 and its product Ang1-7 as counter balanced components of RAS are not defined in asthma, although other RAS components are widely studied.…”

Section: Introductionmentioning

confidence: 99%

“…It targets several tissues such as the brain, pituitary gland, heart, blood vessels, liver, kidneys, and adrenal glands (1,2). RAS includes different enzymes that have critical importance in the pathophysiological processes of several diseases (3,4). Renin is the key enzyme of RAS and converts inactive angiotensinogen (AGT) to angiotensinI (AngI) (5,6).…”

Section: Introductionmentioning

confidence: 99%

Evaluation of Serum Levels of Renin Angiotensin System Components in Asthmatic Patients

Ayada¹,

Toru²,

Genç³

et al. 2015

Erciyes Med J

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Objective: Asthma is a chronic inflammatory lung disease. The renin-angiotensin system (RAS) targets several tissues and maintains fluid homeostasis. It is also known that RAS plays a role in inflammatory processes. Angiotensin-converting enzyme (ACE) and its product angiotensin II (AngII), which are the components of RAS, regulate the known effects of RAS. The other components of RAS, ACE2 and its product Ang 1-7, regulate the counter-effects of RAS. That is why the activation or inhibition of RAS can offer new therapeutic strategies for treating several diseases. We aimed to investigate the serum level of RAS components such as angiotensinogen (AGT), ACE, AngII, ACE2, and Ang 1-7 in asthma and control groups. Materials and Methods:This study was performed on 27 asthma and 23 healthy individuals. The serum levels of AGT, ACE, AngII, ACE2, and Ang 1-7 were measured by human enzyme-linked immunosorbent assay (ELISA) kits.Results: There were no statistically significant differences for the serum levels of AGT and ACE between the groups. The serum levels of AngII, ACE2, and Ang 1-7 were significanlty higher in the asthma group than those in the control group. Conclusion:Our results indicate that two tails of RAS, i.e., the ACE and ACE2 pathways, are activated in asthma compared to are activated more in the asthma group than in the control group. We suppose that the activation of ACE2 tail of RAS occurs because of the homeostatic balance requirements of this system. We believe that the activation of ACE2 pathway, in addition to the inhibition of the ACE pathway, can provide clinical benefits in treating asthma.

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“…Studies demonstrated that ACE2 and ANG-(1-7) may exert protective effects in kinds of lung diseases, 4,5,14) which effects during the progression of PF were being intensively investigated.…”

mentioning

confidence: 99%

Osthole Alleviates Bleomycin-Induced Pulmonary Fibrosis <i>via</i> Modulating Angiotensin-Converting Enzyme 2/Angiotensin-(1–7) Axis and Decreasing Inflammation Responses in Rats

Hao

Liu

2016

Biological & Pharmaceutical Bulletin

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Studies have shown that angiotensin-converting enzyme 2 (ACE2) plays modulating roles in lung pathophysiology, including pulmonary fibrosis (PF) and acute lung injury. Pulmonary fibrosis is a common complication in these interstitial lung diseases, and PF always has a poor prognosis and short survival. To date, there are few promising methods for treating PF, and they are invariably accompanied by severe side effects. Recent studies have showed that the traditional Chinese herbal extract, osthole, had beneficial effects on lipopolysaccharide (LPS) induced acute lung injury (ALI) via an ACE2 pathway. Here we further investigated the protective effects of osthole on bleomycin induced pulmonary fibrosis and attempted to determine the underlying mechanism. PF mode rats were induced by bleomycin (BLM) and then subsequently administered osthole. Histopathological analyses were employed to identify PF changes. The results showed that BLM resulted in severe PF and diffuse lung inflammation, together with significant elevation of inflammatory factors and a marked increase in expression of angiotensin II (ANG II) and transforming growth factor-beta 1 (TGF-β1). ACE2 and angiotensin-(1-7) [ANG-(1-7)] were both greatly reduced after BLM administration. Meanwhile, osthole treatment attenuated BLM induced PF and inflammation, decreased the expression of these inflammatory mediators, ANG II, and TGF-β1, and reversed ACE2 and ANG-(1-7) production in rat lungs. We conclude that osthole may exert beneficial effects on BLM induced PF in rats, perhaps via modulating the ACE2/ANG-(1-7) axis and inhibiting lung inflammation pathways.

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Angiotensin-converting enzyme 2 in lung diseases

Cited by 375 publications

References 61 publications

ApoE-Deficient Mice on Cholate-Containing High-Fat Diet Reveal a Pathology Similar to Lung Sarcoidosis

ApoE-Deficient Mice on Cholate-Containing High-Fat Diet Reveal a Pathology Similar to Lung Sarcoidosis

Evaluation of Serum Levels of Renin Angiotensin System Components in Asthmatic Patients

Osthole Alleviates Bleomycin-Induced Pulmonary Fibrosis <i>via</i> Modulating Angiotensin-Converting Enzyme 2/Angiotensin-(1–7) Axis and Decreasing Inflammation Responses in Rats

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