FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2900830663> ?p ?o ?g. }

• W2900830663 endingPage "3764" @default.
• W2900830663 startingPage "3764" @default.
• W2900830663 abstract "The mineralocorticoid hormone aldosterone regulates sodium and potassium homeostasis but also adversely modulates the maladaptive process of cardiac adverse remodeling post-myocardial infarction. Through activation of its mineralocorticoid receptor (MR), a classic steroid hormone receptor/transcription factor, aldosterone promotes inflammation and fibrosis of the heart, the vasculature, and the kidneys. This is why MR antagonists reduce morbidity and mortality of heart disease patients and are part of the mainstay pharmacotherapy of advanced human heart failure. A plethora of animal studies using cell type–specific targeting of the MR gene have established the importance of MR signaling and function in cardiac myocytes, vascular endothelial and smooth muscle cells, renal cells, and macrophages. In terms of its signaling properties, the MR is distinct from nuclear receptors in that it has, in reality, two physiological hormonal agonists: not only aldosterone but also cortisol. In fact, in several tissues, including in the myocardium, cortisol is the primary hormone activating the MR. There is a considerable amount of evidence indicating that the effects of the MR in each tissue expressing it depend on tissue- and ligand-specific engagement of molecular co-regulators that either activate or suppress its transcriptional activity. Identification of these co-regulators for every ligand that interacts with the MR in the heart (and in other tissues) is of utmost importance therapeutically, since it can not only help elucidate fully the pathophysiological ramifications of the cardiac MR’s actions, but also help design and develop novel better MR antagonist drugs for heart disease therapy. Among the various proteins the MR interacts with are molecules involved in cardiac G protein-coupled receptor (GPCR) signaling. This results in a significant amount of crosstalk between GPCRs and the MR, which can affect the latter’s activity dramatically in the heart and in other cardiovascular tissues. This review summarizes the current experimental evidence for this GPCR-MR crosstalk in the heart and discusses its pathophysiological implications for cardiac adverse remodeling as well as for heart disease therapy. Novel findings revealing non-conventional roles of GPCR signaling molecules, specifically of GPCR-kinase (GRK)-5, in cardiac MR regulation are also highlighted." @default.
• W2900830663 created "2018-11-29" @default.
• W2900830663 creator A5004231521 @default.
• W2900830663 creator A5024688470 @default.
• W2900830663 creator A5027091088 @default.
• W2900830663 creator A5032748291 @default.
• W2900830663 creator A5061897885 @default.
• W2900830663 creator A5066444124 @default.
• W2900830663 creator A5076699689 @default.
• W2900830663 date "2018-11-27" @default.
• W2900830663 modified "2023-10-02" @default.
• W2900830663 title "Novel Insights into the Crosstalk between Mineralocorticoid Receptor and G Protein-Coupled Receptors in Heart Adverse Remodeling and Disease" @default.
• W2900830663 cites W1509389952 @default.
• W2900830663 cites W1965301500 @default.
• W2900830663 cites W1973138130 @default.
• W2900830663 cites W1974109860 @default.
• W2900830663 cites W1982096684 @default.
• W2900830663 cites W1985146730 @default.
• W2900830663 cites W1990001636 @default.
• W2900830663 cites W1997218996 @default.
• W2900830663 cites W2000719141 @default.
• W2900830663 cites W2001367511 @default.
• W2900830663 cites W2005104548 @default.
• W2900830663 cites W2005611207 @default.
• W2900830663 cites W2007587514 @default.
• W2900830663 cites W2011309117 @default.
• W2900830663 cites W2011652462 @default.
• W2900830663 cites W2013495761 @default.
• W2900830663 cites W2013672040 @default.
• W2900830663 cites W2017851269 @default.
• W2900830663 cites W2019330476 @default.
• W2900830663 cites W2020932145 @default.
• W2900830663 cites W2023402651 @default.
• W2900830663 cites W2026493203 @default.
• W2900830663 cites W2026963831 @default.
• W2900830663 cites W2027163029 @default.
• W2900830663 cites W2030020451 @default.
• W2900830663 cites W2034735889 @default.
• W2900830663 cites W2035140438 @default.
• W2900830663 cites W2035575900 @default.
• W2900830663 cites W2036043627 @default.
• W2900830663 cites W2037481669 @default.
• W2900830663 cites W2041819768 @default.
• W2900830663 cites W2049772614 @default.
• W2900830663 cites W2053964593 @default.
• W2900830663 cites W2055723958 @default.
• W2900830663 cites W2059152796 @default.
• W2900830663 cites W2059349901 @default.
• W2900830663 cites W2067956701 @default.
• W2900830663 cites W2068638594 @default.
• W2900830663 cites W2070551632 @default.
• W2900830663 cites W2071806226 @default.
• W2900830663 cites W2075323044 @default.
• W2900830663 cites W2085491937 @default.
• W2900830663 cites W2085599941 @default.
• W2900830663 cites W2087515469 @default.
• W2900830663 cites W2089619186 @default.
• W2900830663 cites W2093901402 @default.
• W2900830663 cites W2098711981 @default.
• W2900830663 cites W2100794825 @default.
• W2900830663 cites W2101877864 @default.
• W2900830663 cites W2102041759 @default.
• W2900830663 cites W2106052381 @default.
• W2900830663 cites W2106173943 @default.
• W2900830663 cites W2109689484 @default.
• W2900830663 cites W2111001345 @default.
• W2900830663 cites W2114899132 @default.
• W2900830663 cites W2117451333 @default.
• W2900830663 cites W2122269095 @default.
• W2900830663 cites W2122456701 @default.
• W2900830663 cites W2123801122 @default.
• W2900830663 cites W2124371332 @default.
• W2900830663 cites W2130336115 @default.
• W2900830663 cites W2130963272 @default.
• W2900830663 cites W2131715702 @default.
• W2900830663 cites W2133493473 @default.
• W2900830663 cites W2134527631 @default.
• W2900830663 cites W2135721157 @default.
• W2900830663 cites W2137517013 @default.
• W2900830663 cites W2138685167 @default.
• W2900830663 cites W2140212665 @default.
• W2900830663 cites W2145584016 @default.
• W2900830663 cites W2148598424 @default.
• W2900830663 cites W2149081700 @default.
• W2900830663 cites W2150011193 @default.
• W2900830663 cites W2153020609 @default.
• W2900830663 cites W2156250141 @default.
• W2900830663 cites W2156460525 @default.
• W2900830663 cites W2160937709 @default.
• W2900830663 cites W2161356489 @default.
• W2900830663 cites W2162008803 @default.
• W2900830663 cites W2166001681 @default.
• W2900830663 cites W2168061260 @default.
• W2900830663 cites W2168588787 @default.
• W2900830663 cites W2168671091 @default.
• W2900830663 cites W2169595007 @default.
• W2900830663 cites W2171671716 @default.
• W2900830663 cites W2180491396 @default.

• next