The DOI matches its Crossref record; 25 of the 25 references it cites were found in a registry or an index.
Pressure-independent cardiac hypertrophy in mice with cardiomyocyte-restricted inactivation of the atrial natriuretic peptide receptor guanylyl cyclase-A
Open accessAbstract
Cardiac hypertrophy is a common and often lethal complication of arterial hypertension. Atrial natriuretic peptide (ANP) has been postulated to exert local antihypertrophic effects in the heart. Thus, a loss of function of the ANP receptor guanylyl cyclase-A (GC-A) might contribute to the increased propensity to cardiac hypertrophy, although a causative role in vivo has not been definitively demonstrated. To test whether local ANP modulates cardiomyocyte growth, we inactivated the GC-A gene selectively in cardiomyocytes by homologous loxP/Cre-mediated recombination. Thereby we have circumvented the systemic, hypertensive phenotype associated with germline inactivation of GC-A. Mice with cardiomyocyte-restricted GC-A deletion exhibited mild cardiac hypertrophy, markedly increased mRNA expression of cardiac hypertrophy markers such as ANP (fivefold), alpha-skeletal actin (1.7-fold), and beta-myosin heavy chain (twofold), and increased systemic circulating ANP levels. Their blood pressure was 7-10 mmHg below normal, probably because of the elevated systemic levels and endocrine actions of ANP. Furthermore, cardiac hypertrophic responses to aortic constriction were enhanced and accompanied by marked deterioration of cardiac function. This phenotype is consistent with a local function of the ANP/GC-A system to moderate the molecular program of cardiac hypertrophy.
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Diverse biological actions of atrial natriuretic peptide
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Self-citationCardiac fibrosis in mice lacking brain natriuretic peptide
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Self-citationDwarfism and early death in mice lacking C-type natriuretic peptide
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Cited by
Hypertrophy of the Heart: A New Therapeutic Target?
Frey, N., Katus, H. A., Olson, E. N., & Hill, J. A. (2004) · Circulation · doi:10.1161/01.cir.0000120390.68287.bb · Cited by 851
Role of Oxidative Stress in Cardiac Hypertrophy and Remodeling
Takimoto, E., & Kass, D. A. (2007) · Hypertension · doi:10.1161/01.hyp.0000254415.31362.a7 · Cited by 770
Molecular Pathways Underlying Cardiac Remodeling During Pathophysiological Stimulation
Kehat, I., & Molkentin, J. D. (2010) · Circulation · doi:10.1161/circulationaha.110.942268 · Cited by 592
Cellular and molecular pathobiology of heart failure with preserved ejection fraction
Mishra, S., & Kass, D. A. (2021) · Nature Reviews Cardiology · doi:10.1038/s41569-020-00480-6 · Cited by 417
Hilfiker-Kleiner, D., Hilfiker, A., Fuchs, M., Kaminski, K., Schaefer, A., Schieffer, B., Hillmer, A., Schmiedl, A., Ding, Z., Podewski, E., et al. (2004) · Circulation Research · doi:10.1161/01.res.0000134921.50377.61 · Cited by 385
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Metadata
- Authors
- Holtwick, R., van Eickels, M., Skryabin, B. V., Baba, H. A., Bubikat, A., Begrow, F., Schneider, M. D., Garbers, D. L., & Kuhn, M.
- Venue
- Journal of Clinical Investigation
- Published
- 2003-05-01
- Volume
- 111
- Issue
- 9
- Pages
- 1399-1407
- ISSN
- 0021-9738 (ISSN-L)
- OpenAlex
- W2011780678
- Cited by
- 340
- References
- 25
- FWCI
- 18.44
- Type
- journal article
- Language
- en
- Open access
- bronze
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- CoChat. (2026). Citation check: Pressure-independent cardiac hypertrophy in mice with cardiomyocyte-restricted inactivation of the atrial natriuretic peptide receptor guanylyl cyclase-A. https://app.cochat.ai/papers/10.1172/jci17061
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- Holtwick, R., van Eickels, M., Skryabin, B. V., Baba, H. A., Bubikat, A., Begrow, F., Schneider, M. D., Garbers, D. L., & Kuhn, M. (2003). Pressure-independent cardiac hypertrophy in mice with cardiomyocyte-restricted inactivation of the atrial natriuretic peptide receptor guanylyl cyclase-A. Journal of Clinical Investigation. https://doi.org/10.1172/jci17061
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