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The DOI matches its Crossref record; 105 of the 105 references it cites were found in a registry or an index.

Neurohormonal activation in heart failure with reduced ejection fraction

Open access
Hartupee, Justin, Mann, Douglas L.·2017·Nature Reviews Cardiology

Abstract

Heart failure with reduced ejection fraction (HFrEF) develops when cardiac output falls as a result of cardiac injury. The most well-recognized of the compensatory homeostatic responses to a fall in cardiac output are activation of the sympathetic nervous system and the renin–angiotensin–aldosterone system (RAAS). In the short term, these 'neurohormonal' systems induce a number of changes in the heart, kidneys, and vasculature that are designed to maintain cardiovascular homeostasis. However, with chronic activation, these responses result in haemodynamic stress and exert deleterious effects on the heart and the circulation. Neurohormonal activation is now known to be one of the most important mechanisms underlying the progression of heart failure, and therapeutic antagonism of neurohormonal systems has become the cornerstone of contemporary pharmacotherapy for heart failure. In this Review, we discuss the effects of neurohormonal activation in HFrEF and highlight the mechanisms by which these systems contribute to disease progression.

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Metadata

Authors
Hartupee, J., & Mann, D. L.
Venue
Nature Reviews Cardiology
Published
2016-10-06
Volume
14
Issue
1
Pages
30-38
ISSN
  • 1759-5002 (ISSN-L)
  • 1759-5010
OpenAlex
W2529406298
Cited by
709
References
105
FWCI
4.68
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: Neurohormonal activation in heart failure with reduced ejection fraction. https://app.cochat.ai/papers/10.1038/nrcardio.2016.163
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Hartupee, J., & Mann, D. L. (2017). Neurohormonal activation in heart failure with reduced ejection fraction. Nature Reviews Cardiology. https://doi.org/10.1038/nrcardio.2016.163

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