The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.
The Angiotensin-Converting Enzyme 2/Angiogenesis-(1–7)/Mas Axis Confers Cardiopulmonary Protection against Lung Fibrosis and Pulmonary Hypertension
Open accessAbstract
RATIONALE: An activated vasoconstrictive, proliferative, and fibrotic axis of the renin angiotensin system (angiotensin-converting enzyme [ACE]/angiotensin [Ang]II/AngII type 1 receptor) has been implicated in the pathophysiology of pulmonary fibrosis (PF) and pulmonary hypertension (PH). The recent discovery of a counterregulatory axis of the renin angiotensin system composed of ACE2/Ang-(1-7)/Mas has led us to examine the role of this vasoprotective axis on such disorders. OBJECTIVES: We hypothesized that Ang-(1-7) treatment would exert protective effects against PF and PH. METHODS: Lentiviral packaged Ang-(1-7) fusion gene or ACE2 cDNA was intratracheally administered into the lungs of male Sprague Dawley rats. Two weeks after gene transfer, animals received bleomycin (2.5 mg/kg). In a subsequent study, animals were administered monocrotaline (MCT, 50 mg/kg). MEASUREMENTS AND MAIN RESULTS: In the PF study, bleomycin administration resulted in a significant increase in right ventricular systolic pressure, which was associated with the development of right ventricular hypertrophy. The lungs of these animals also exhibited excessive collagen deposition, decreased expression of ACE and ACE2, increased mRNA levels for transforming growth factor β and other proinflammatory cytokines, and increased protein levels of the AT₁R. Overexpression of Ang-(1-7) significantly prevented all the above-mentioned pathophysiological conditions. Similar protective effects were also obtained with ACE2 overexpression. In the PH study, rats injected with MCT developed elevated right ventricular systolic pressure, right ventricular hypertrophy, right ventricular fibrosis, and pulmonary vascular remodeling, all of which were attenuated by Ang-(1-7) overexpression. Blockade of the Mas receptor abolished the beneficial effects of Ang-(1-7) against MCT-induced PH. CONCLUSIONS: Our observations demonstrate a cardiopulmonary protective role for the ACE2/Ang-(1-7)/Mas axis in the treatment of lung disorders.
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A crucial role of angiotensin converting enzyme 2 (ACE2) in SARS coronavirus–induced lung injury
Kuba, K., Imai, Y., Rao, S., Gao, H., Guo, F., Guan, B., Huan, Y., Yang, P., Zhang, Y., Deng, W., et al. (2005) · Nature Medicine · doi:10.1038/nm1267 · Cited by 3,445
Cited by
The ACE2/angiotensin-(1-7)/MAS Axis of the renin-angiotensin system: focus on angiotensin-(1-7)
Santos, R. A. S., Sampaio, W. O., Alzamora, A. C., Motta-Santos, D., Alenina, N., Bader, M., & Campagnole-Santos, M. J. (2018) · Physiological Reviews · doi:10.1152/physrev.00023.2016 · Cited by 1,144
Self-citationDysregulated Renin–Angiotensin–Aldosterone System Contributes to Pulmonary Arterial Hypertension
de Man, F. S., Tu, L., Handoko, M. L., Rain, S., Ruiter, G., François, C., Schalij, I., Dorfmüller, P., Simonneau, G., Fadel, E., et al. (2012) · American Journal of Respiratory and Critical Care Medicine · doi:10.1164/rccm.201203-0411oc · Cited by 346
Varga, J., Trojanowska, M., & Kuwana, M. (2017) · Journal of Scleroderma and Related Disorders · doi:10.5301/jsrd.5000249 · Cited by 323
Sarzani, R., Giulietti, F., Di Pentima, C., Giordano, P., & Spannella, F. (2020) · American Journal of Physiology-Lung Cellular and Molecular Physiology · doi:10.1152/ajplung.00189.2020 · Cited by 86
Schrom, E., Huber, M., Aneja, M., Dohmen, C., Emrich, D., Geiger, J., Hasenpusch, G., Herrmann-Janson, A., Kretzschmann, V., Mykhailyk, O., et al. (2017) · Molecular Therapy — Nucleic Acids · doi:10.1016/j.omtn.2017.04.006 · Cited by 69
“Establishing ACE2 translation in type I AECs could not be achieved by recombinant protein therapy(21) or lentiviral-mediated ACE2 overexpression.(23)”
BackgroundMethod
Metadata
- Authors
- Shenoy, V., Ferreira, A. J., Qi, Y., Fraga-Silva, R. A., Díez-Freire, C., Dooies, A., Jun, J. Y., Sriramula, S., Mariappan, N., Pourang, D., Venugopal, C. S., Francis, J., Reudelhuber, T., Santos, R. A., Patel, J. M., Raizada, M. K., & Katovich, M. J.
- Venue
- American Journal of Respiratory and Critical Care Medicine
- Publisher
- Oxford University Press (OUP)
- Published
- 2010-10-15
- Volume
- 182
- Issue
- 8
- Pages
- 1065-1072
- ISSN
- 1073-449X (ISSN-L)
- 1535-4970
- OpenAlex
- W2015945747
- Cited by
- 281
- References
- 1
- FWCI
- 10.63
- Type
- journal article
- Language
- en
- Open access
- green
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- Shenoy, V., Ferreira, A. J., Qi, Y., Fraga-Silva, R. A., Díez-Freire, C., Dooies, A., Jun, J. Y., Sriramula, S., Mariappan, N., Pourang, D., Venugopal, C. S., Francis, J., Reudelhuber, T., Santos, R. A., Patel, J. M., Raizada, M. K., & Katovich, M. J. (2010). The Angiotensin-Converting Enzyme 2/Angiogenesis-(1–7)/Mas Axis Confers Cardiopulmonary Protection against Lung Fibrosis and Pulmonary Hypertension. American Journal of Respiratory and Critical Care Medicine. https://doi.org/10.1164/rccm.200912-1840oc
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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