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Cited by 308

The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.

Impaired Heart Contractility in Apelin Gene–Deficient Mice Associated With Aging and Pressure Overload

Open access
Kuba, Keiji, Zhang, Liyong, Imai, Yumiko, Arab, Sara, Chen, Manyin, Maekawa, Yuichiro, Leschnik, Michael, Leibbrandt, Andreas, Markovic, Mato, Schwaighofer, Julia, Beetz, Nadine, Musialek, Renata, Neely, G. Greg, Komnenovic, Vukoslav, Kolm, Ursula, Metzler, Bernhard, Ricci, Romeo, Hara, Hiromitsu, Meixner, Arabella, Nghiem, Mai, Chen, Xin, Dawood, Fayez, Wong, Kit Man, Sarao, Renu, Cukerman, Eva, Kimura, Akinori, Hein, Lutz, Thalhammer, Johann, Liu, Peter P., Penninger, Josef M.·2007·Circulation Research

Abstract

Apelin constitutes a novel endogenous peptide system suggested to be involved in a broad range of physiological functions, including cardiovascular function, heart development, control of fluid homeostasis, and obesity. Apelin is also a catalytic substrate for angiotensin-converting enzyme 2, the key severe acute respiratory syndrome receptor. The in vivo physiological role of Apelin is still elusive. Here we report the generation of Apelin gene–targeted mice. Apelin mutant mice are viable and fertile, appear healthy, and exhibit normal body weight, water and food intake, heart rates, and heart morphology. Intriguingly, aged Apelin knockout mice developed progressive impairment of cardiac contractility associated with systolic dysfunction in the absence of histological abnormalities. We also report that pressure overload induces upregulation of Apelin expression in the heart. Importantly, in pressure overload–induced heart failure, loss of Apelin did not significantly affect the hypertrophy response, but Apelin mutant mice developed progressive heart failure. Global gene expression arrays and hierarchical clustering of differentially expressed genes in hearts of banded Apelin −/y and Apelin +/y mice showed concerted upregulation of genes involved in extracellular matrix remodeling and muscle contraction. These genetic data show that the endogenous peptide Apelin is crucial to maintain cardiac contractility in pressure overload and aging.

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Metadata

Authors
Kuba, K., Zhang, L., Imai, Y., Arab, S., Chen, M., Maekawa, Y., Leschnik, M., Leibbrandt, A., Markovic, M., Schwaighofer, J., Beetz, N., Musialek, R., Neely, G. G., Komnenovic, V., Kolm, U., Metzler, B., Ricci, R., Hara, H., Meixner, A., Nghiem, M., Chen, X., Dawood, F., Wong, K. M., Sarao, R., Cukerman, E., Kimura, A., Hein, L., Thalhammer, J., Liu, P. P., & Penninger, J. M.
Venue
Circulation Research
Published
2007-08-17
Volume
101
Issue
4
Pages
e32-42
ISSN
  • 0009-7330 (ISSN-L)
  • 1524-4571
OpenAlex
W2127087522
Cited by
308
References
6
FWCI
11.36
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: Impaired Heart Contractility in Apelin Gene–Deficient Mice Associated With Aging and Pressure Overload. https://app.cochat.ai/papers/10.1161/circresaha.107.158659
The paper
Kuba, K., Zhang, L., Imai, Y., Arab, S., Chen, M., Maekawa, Y., Leschnik, M., Leibbrandt, A., Markovic, M., Schwaighofer, J., Beetz, N., Musialek, R., Neely, G. G., Komnenovic, V., Kolm, U., Metzler, B., Ricci, R., Hara, H., Meixner, A., . . . Penninger, J. M. (2007). Impaired Heart Contractility in Apelin Gene–Deficient Mice Associated With Aging and Pressure Overload. Circulation Research. https://doi.org/10.1161/circresaha.107.158659

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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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