FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2008490829> ?p ?o ?g. }

• W2008490829 endingPage "1277" @default.
• W2008490829 startingPage "1275" @default.
• W2008490829 abstract "Cardiovascular disease remains as the leading cause of death throughout the industrialized nations of the world. Central to this statistic is our current inability to effectively repair or otherwise reverse severe forms of cardiac dysfunction and pathologic remodeling that characterizes a failing heart. In response to hypertension, ischemic disease, valvular insufficiency, viral myocarditis, and genetic mutations in sacomeric proteins, the myocardium undergoes a hypertrophic growth phase as a compensatory measure aimed at maintaining cardiac output (1). However, longstanding cardiac hypertrophy often precipitates the development of more serious complications such as sudden death, fibrotic restrictive cardiomyopathy, dilated cardiomyopathy, and overt failure (2). Given the relatively poor clinical prognosis associated with end-stage heart failure, much investigation has focused on understanding the molecular underpinnings associated with the preceding hypertrophic remodeling stage. Indeed, a number of signaling networks have been identified that directly regulate the hypertrophic growth of cardiac myocytes (3). For example, neuroendocrine factors and/or intrinsic stretch-sensitive sensors, which signal through G protein–coupled receptors, receptor tyrosine kinases, or directly to second messengers, are thought to function as the initiating stimulus for the hypertrophic response (Figure ​(Figure1).1). These upstream events promote signal transduction through a network of kinases and phosphatases thereby coordinating an increase in gene expression, total protein production and/or accumulation, and rRNA content, thus driving the hypertrophic growth of myocytes. However, as is common to most biological response systems, a counter-regulatory network typically exists that buffers or antagonizes the forward cascade to permit selective reversal or graded responsiveness. Indeed, in this issue of the JCI, the article by Holtwick and colleagues provides definitive evidence for the existence of an antihypertrophic regulatory circuit within cardiac myocytes that functions to directly antagonize the hypertrophic growth response (4). This antihypertrophic regulatory circuit consists of the secreted atrial and B-type natriuretic peptides (ANP and BNP, respectively), and the ANP receptor guanylyl cyclase-A (GC-A).Figure 1Cardiac myocytes have signaling pathways that agonize and antagonize hypertrophic growth. Neuroendocrine factors typically stimulate G protein–coupled receptors (GPCRs) and/or receptor tyrosine kinases (RTKs), which activate an array of intermediate ..." @default.
• W2008490829 created "2016-06-24" @default.
• W2008490829 creator A5075550603 @default.
• W2008490829 date "2003-05-01" @default.
• W2008490829 modified "2023-09-25" @default.
• W2008490829 title "A friend within the heart: natriuretic peptide receptor signaling" @default.
• W2008490829 cites W1533077678 @default.
• W2008490829 cites W1557787993 @default.
• W2008490829 cites W1964541624 @default.
• W2008490829 cites W1983692570 @default.
• W2008490829 cites W1984893737 @default.
• W2008490829 cites W1995573946 @default.
• W2008490829 cites W2006025730 @default.
• W2008490829 cites W2011632934 @default.
• W2008490829 cites W2011780678 @default.
• W2008490829 cites W2024515082 @default.
• W2008490829 cites W2030165232 @default.
• W2008490829 cites W2079509424 @default.
• W2008490829 cites W2093695309 @default.
• W2008490829 cites W2103751591 @default.
• W2008490829 cites W2109488054 @default.
• W2008490829 cites W2114425457 @default.
• W2008490829 cites W2118435007 @default.
• W2008490829 cites W2120553703 @default.
• W2008490829 cites W2130678592 @default.
• W2008490829 cites W2158344911 @default.
• W2008490829 cites W2298790217 @default.
• W2008490829 cites W2334499091 @default.
• W2008490829 cites W4238717174 @default.
• W2008490829 doi "https://doi.org/10.1172/jci18389" @default.
• W2008490829 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/154452" @default.
• W2008490829 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/12727915" @default.
• W2008490829 hasPublicationYear "2003" @default.
• W2008490829 type Work @default.
• W2008490829 sameAs 2008490829 @default.
• W2008490829 citedByCount "70" @default.
• W2008490829 countsByYear W20084908292012 @default.
• W2008490829 countsByYear W20084908292013 @default.
• W2008490829 countsByYear W20084908292014 @default.
• W2008490829 countsByYear W20084908292015 @default.
• W2008490829 countsByYear W20084908292016 @default.
• W2008490829 countsByYear W20084908292017 @default.
• W2008490829 countsByYear W20084908292018 @default.
• W2008490829 countsByYear W20084908292019 @default.
• W2008490829 countsByYear W20084908292020 @default.
• W2008490829 countsByYear W20084908292022 @default.
• W2008490829 crossrefType "journal-article" @default.
• W2008490829 hasAuthorship W2008490829A5075550603 @default.
• W2008490829 hasBestOaLocation W20084908291 @default.
• W2008490829 hasConcept C126322002 @default.
• W2008490829 hasConcept C134018914 @default.
• W2008490829 hasConcept C170493617 @default.
• W2008490829 hasConcept C2775915353 @default.
• W2008490829 hasConcept C2778198053 @default.
• W2008490829 hasConcept C71924100 @default.
• W2008490829 hasConcept C86803240 @default.
• W2008490829 hasConcept C8741621 @default.
• W2008490829 hasConceptScore W2008490829C126322002 @default.
• W2008490829 hasConceptScore W2008490829C134018914 @default.
• W2008490829 hasConceptScore W2008490829C170493617 @default.
• W2008490829 hasConceptScore W2008490829C2775915353 @default.
• W2008490829 hasConceptScore W2008490829C2778198053 @default.
• W2008490829 hasConceptScore W2008490829C71924100 @default.
• W2008490829 hasConceptScore W2008490829C86803240 @default.
• W2008490829 hasConceptScore W2008490829C8741621 @default.
• W2008490829 hasIssue "9" @default.
• W2008490829 hasLocation W20084908291 @default.
• W2008490829 hasLocation W20084908292 @default.
• W2008490829 hasLocation W20084908293 @default.
• W2008490829 hasLocation W20084908294 @default.
• W2008490829 hasOpenAccess W2008490829 @default.
• W2008490829 hasPrimaryLocation W20084908291 @default.
• W2008490829 hasRelatedWork W1972033663 @default.
• W2008490829 hasRelatedWork W1996846474 @default.
• W2008490829 hasRelatedWork W2018368842 @default.
• W2008490829 hasRelatedWork W2033472167 @default.
• W2008490829 hasRelatedWork W2034583712 @default.
• W2008490829 hasRelatedWork W2052453588 @default.
• W2008490829 hasRelatedWork W2063619316 @default.
• W2008490829 hasRelatedWork W2071457715 @default.
• W2008490829 hasRelatedWork W2169225653 @default.
• W2008490829 hasRelatedWork W2414846389 @default.
• W2008490829 hasVolume "111" @default.
• W2008490829 isParatext "false" @default.
• W2008490829 isRetracted "false" @default.
• W2008490829 magId "2008490829" @default.
• W2008490829 workType "article" @default.