The contribution of the AT1 receptor to erythropoiesis.

Autor: Rodrigues AF; Max Delbrück Center (MDC), Berlin, Germany; German Center for Cardiovascular Research (DZHK), Partner Site Berlin, Germany. Electronic address: andrefelipe.rodrigues@mdc-berlin.de., Bader M; Max Delbrück Center (MDC), Berlin, Germany; German Center for Cardiovascular Research (DZHK), Partner Site Berlin, Germany; Charité Universitätsmedizin Berlin, Berlin, Germany; Institute for Biology, University of Lübeck, Lübeck, Germany. Electronic address: mbader@mdc-berlin.de.
Jazyk: angličtina
Zdroj: Biochemical pharmacology [Biochem Pharmacol] 2023 Nov; Vol. 217, pp. 115805. Date of Electronic Publication: 2023 Sep 14.
DOI: 10.1016/j.bcp.2023.115805
Abstrakt: The renin-angiotensin system (RAS) comprises a broad set of functional peptides and receptors that play a role in cardiovascular homeostasis and contribute to cardiovascular pathologies. Angiotensin II (Ang II) is the most potent peptide hormone produced by the RAS due to its high abundance and its strong and pleiotropic impact on the cardiovascular system. Formation of Ang II takes place in the bloodstream and additionally in tissues in the so-called local RAS. Of the two Ang II receptors (AT1 and AT2) that Ang II binds to, AT1 is the most expressed throughout the mammalian body. AT1 expression is not restricted to cells of the cardiovascular system but in fact AT1 protein is found in nearly all organs, hence, Ang II takes part in several modulatory physiological processes one of which is erythropoiesis. In this review, we present multiple evidence supporting that Ang II modulates physiological and pathological erythropoiesis processes trough the AT1 receptor. Cumulative evidence indicates that Ang II by three distinct mechanisms influences erythropoiesis: 1) stimulation of renal erythropoietin synthesis; 2) direct action on bone marrow precursor cells; and 3) modulation of sympathetic nerve activity to the bone marrow. The text highlights clinical and preclinical evidence focusing on mechanistic studies using rodent models.
Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2023 Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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