The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.
What Is the Role of β-Adrenergic Signaling in Heart Failure?
Abstract
This review addresses open questions about the role of β-adrenergic receptors in cardiac function and failure. Cardiomyocytes express all three β-adrenergic receptor subtypes—β 1 , β 2 , and, at least in some species, β 3 . The β 1 subtype is the most prominent one and is mainly responsible for positive chronotropic and inotropic effects of catecholamines. The β 2 subtype also increases cardiac function, but its ability to activate nonclassical signaling pathways suggests a function distinct from the β 1 subtype. In heart failure, the sympathetic system is activated, cardiac β-receptor number and function are decreased, and downstream mechanisms are altered. However, in spite of a wealth of data, we still do not know whether and to what extent these alterations are adaptive/protective or detrimental, or both. Clinically, β-adrenergic antagonists represent the most important advance in heart failure therapy, but it is still debated whether they act by blocking or by resensitizing the β-adrenergic receptor system. Newer experimental therapeutic strategies aim at the receptor desensitization machinery and at downstream signaling steps.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Tissue distribution of beta 3-adrenergic receptor mRNA in man
Krief, S., Lönnqvist, F., Raimbault, S., Baude, B., Van Spronsen, A., Arner, P., Strosberg, A. D., Ricquier, D., & Emorine, L. J. (1993) · Journal of Clinical Investigation · doi:10.1172/jci116191 · Cited by 528
del Monte, F., Williams, E., Lebeche, D., Schmidt, U., Rosenzweig, A., Gwathmey, J. K., Lewandowski, E. D., & Hajjar, R. J. (2001) · Circulation · doi:10.1161/hc3601.095574 · Cited by 382
Ostrom, R. S., Gregorian, C., Drenan, R. M., Xiang, Y., Regan, J. W., & Insel, P. A. (2001) · Journal of Biological Chemistry · doi:10.1074/jbc.m105348200 · Cited by 250
Cited by
The Sympathetic Nervous System in Heart Failure
Triposkiadis, F., Karayannis, G., Giamouzis, G., Skoularigis, J., Louridas, G., & Butler, J. (2009) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2009.05.015 · Cited by 978
Reducing safety-related drug attrition: the use of in vitro pharmacological profiling
Bowes, J., Brown, A. J., Hamon, J., Jarolimek, W., Sridhar, A., Waldron, G., & Whitebread, S. (2012) · Nature Reviews Drug Discovery · doi:10.1038/nrd3845 · Cited by 748
Regulation, signaling, and physiological functions of G-Proteins
Syrovatkina, V., Alegre, K. O., Dey, R., & Huang, X.-Y. (2016) · Journal of Molecular Biology · doi:10.1016/j.jmb.2016.08.002 · Cited by 498
Signaling effectors underlying pathologic growth and remodeling of the heart
van Berlo, J. H., Maillet, M., & Molkentin, J. D. (2013) · Journal of Clinical Investigation · doi:10.1172/jci62839 · Cited by 445
Morimoto, T., Sunagawa, Y., Kawamura, T., Takaya, T., Wada, H., Nagasawa, A., Komeda, M., Fujita, M., Shimatsu, A., Kita, T., et al. (2008) · Journal of Clinical Investigation · doi:10.1172/jci33160 · Cited by 423
Metadata
- Authors
- Lohse, M. J., Engelhardt, S., & Eschenhagen, T.
- Venue
- Circulation Research
- Published
- 2003-11-14
- Volume
- 93
- Issue
- 10
- Pages
- 896-906
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- OpenAlex
- W2138354938
- Cited by
- 764
- References
- 3
- FWCI
- 9.01
- Type
- journal article
- Language
- en
- Open access
- closed
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: What Is the Role of β-Adrenergic Signaling in Heart Failure? https://app.cochat.ai/papers/10.1161/01.res.0000102042.83024.ca
- The paper
- Lohse, M. J., Engelhardt, S., & Eschenhagen, T. (2003). What Is the Role of β-Adrenergic Signaling in Heart Failure? Circulation Research. https://doi.org/10.1161/01.res.0000102042.83024.ca
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
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.
