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Cited by 323

The DOI matches its Crossref record; 29 of the 29 references it cites were found in a registry or an index.

Deletion of Angiotensin-Converting Enzyme 2 Accelerates Pressure Overload-Induced Cardiac Dysfunction by Increasing Local Angiotensin II

Open access
Yamamoto, Koichi, Ohishi, Mitsuru, Katsuya, Tomohiro, Ito, Norihisa, Ikushima, Masashi, Kaibe, Masaharu, Tatara, Yuji, Shiota, Atsushi, Sugano, Sumio, Takeda, Satoshi, Rakugi, Hiromi, Ogihara, Toshio·2006·Hypertension
DOI 10.1161/01.hyp.0000205833.89478.5b
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Abstract

Angiotensin-converting enzyme 2 (ACE2) is a carboxypeptidase that cleaves angiotensin II to angiotensin 1-7. Recently, it was reported that mice lacking ACE2 ( ACE2 −/y mice) exhibited reduced cardiac contractility. Because mechanical pressure overload activates the cardiac renin-angiotensin system, we used ACE2 −/y mice to analyze the role of ACE2 in the response to pressure overload. Twelve-week-old ACE2 −/y mice and wild-type (WT) mice received transverse aortic constriction (TAC) or sham operation. Sham-operated ACE2 −/y mice exhibited normal cardiac function and had morphologically normal hearts. In response to TAC, ACE2 −/y mice developed cardiac hypertrophy and dilatation. Furthermore, their hearts displayed decreased cardiac contractility and increased fetal cardiac gene induction, compared with WT mice. In response to chronic pressure overload, ACE2 −/y mice developed pulmonary congestion and increased incidence of cardiac death compared with WT mice. On a biochemical level, cardiac angiotensin II concentration and activity of mitogen-activated protein (MAP) kinases were markedly increased in ACE2 −/y mice in response to TAC. Administration of candesartan, an AT 1 subtype angiotensin receptor blocker, attenuated the hypertrophic response and suppressed the activation of MAP kinases in ACE2 −/y mice. Activation of MAP kinases in response to angiotensin II was greater in cardiomyocytes isolated from ACE2 −/y mice than in those isolated from WT mice. ACE2 plays an important role in dampening the hypertrophic response to pressure overload mediated by angiotensin II. Disruption of this regulatory function may accelerate cardiac hypertrophy and shorten the transition period from compensated hypertrophy to cardiac failure.

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Metadata

Authors
Yamamoto, K., Ohishi, M., Katsuya, T., Ito, N., Ikushima, M., Kaibe, M., Tatara, Y., Shiota, A., Sugano, S., Takeda, S., Rakugi, H., & Ogihara, T.
Venue
Hypertension
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
2006-04
Volume
47
Issue
4
Pages
718-726
ISSN
  • 0194-911X (ISSN-L)
  • 1524-4563
DOI
10.1161/01.hyp.0000205833.89478.5b
OpenAlex
W2109740270
Cited by
323
References
29
FWCI
14.22
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: Deletion of Angiotensin-Converting Enzyme 2 Accelerates Pressure Overload-Induced Cardiac Dysfunction by Increasing Local Angiotensin II. https://app.cochat.ai/papers/10.1161/01.hyp.0000205833.89478.5b
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Yamamoto, K., Ohishi, M., Katsuya, T., Ito, N., Ikushima, M., Kaibe, M., Tatara, Y., Shiota, A., Sugano, S., Takeda, S., Rakugi, H., & Ogihara, T. (2006). Deletion of Angiotensin-Converting Enzyme 2 Accelerates Pressure Overload-Induced Cardiac Dysfunction by Increasing Local Angiotensin II. Hypertension. https://doi.org/10.1161/01.hyp.0000205833.89478.5b

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.