The DOI matches its Crossref record; 214 of the 214 references it cites were found in a registry or an index.
Endogenous Cardiotonic Steroids: Physiology, Pharmacology, and Novel Therapeutic Targets
Open accessAbstract
Endogenous cardiotonic steroids (CTS), also called digitalis-like factors, have been postulated to play important roles in health and disease for nearly half a century. Recent discoveries, which include the specific identification of endogenous cardenolide (endogenous ouabain) and bufadienolide (marinobufagenin) CTS in humans along with the delineation of an alternative mechanism by which CTS can signal through the Na+/K+-ATPase, have increased the interest in this field substantially. Although CTS were first considered important in the regulation of renal sodium transport and arterial pressure, more recent work implicates these hormones in the regulation of cell growth, differentiation, apoptosis, and fibrosis, the modulation of immunity and of carbohydrate metabolism, and the control of various central nervous functions and even behavior. This review focuses on the physiological interactions between CTS and other regulatory systems that may be important in the pathophysiology of essential hypertension, preeclampsia, end-stage renal disease, congestive heart failure, and diabetes mellitus. Based on our increasing understanding of the regulation of CTS as well as the molecular mechanisms of these hormone increases, we also discuss potential therapeutic strategies.
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Reciprocal Regulation of Endocytosis and Metabolism
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Metadata
- Authors
- Bagrov, A. Y., Shapiro, J. I., & Fedorova, O. V.
- Venue
- Pharmacological Reviews
- Publisher
- Elsevier BV
- Published
- 2009-03
- Volume
- 61
- Issue
- 1
- Pages
- 9-38
- ISSN
- 0031-6997 (ISSN-L)
- OpenAlex
- W2143617499
- Cited by
- 532
- References
- 214
- FWCI
- 21.09
- Type
- journal article
- Language
- en
- Open access
- green
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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).
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