FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W1569088697> ?p ?o ?g. }

• W1569088697 abstract "The prevalence of chronic kidney disease (CKD) is on the rise, and it is estimated that more than 26 million Americans suffer from CKD1. The leading risk factors in the development of CKD are hypertension (HTN), diabetes mellitus (DM) and obesity. Because of the increasing prevalence of these risk factors as well as their frequent coexistence in the same patient, prevention strategies that would be able to decrease the progression of CKD to end stage renal disease (ESRD) are of paramount importance. There is a growing body of evidence showing that the activation of the renin angiotensin aldosterone system (RAAS) plays an important role in the development of cardiovascular and renal disorders2,3. RAAS is one of the key players in human physiology, and under normal physiological conditions it regulates blood pressure homeostasis, water balance, renal function and cellular growth. RAAS consists of a cascade of peptide hormones, with the enzyme renin catalyzing the first step in a cascade leading to the production of angiotensin I (AngI) from a precursor angiotensinogen (Figure 1). The cleavage of angiotensinogen, catalyzed by renin, is the rate-limiting step in RAAS activation. AngI does not possess vasoconstricting abilities, and it is cleaved by angiotensin-converting enzyme (ACE) into active angiotensin II (AngII). AngII binds to angiotensin receptors and exerts powerful vasoconstricting abilities. AngII also activates aldosterone production, and regulates sodium and water reapsorption (Figure 1). The kidneys are one of the major targets for RAAS as evidenced by the robust expression of RAAS components and receptors in the kidney4. Renal effects of AngII include regulation of renal blood flow, glomerular filtration rate (GFR) and sodium and water balance5. Upregulation of renal RAAS has been linked to the development of CKD in both HTN and DM4. Hence, therapies that modulate RAAS have emerged as essential tools in decreasing the progression of CKD. Pharmacological inhibition of RAAS can be obtained via three different mechanisms: 1. Inhibition of conversion of AngI to active AngII via angiotensin I converting enzyme inhibitors (ACEI); 2. Selective inhibition of angiotensin receptor 1 (AR-1) via angiotensin receptor blockers (ARB); 3. Direct inhibition of AngI production via direct rennin inhibitors (DRI)." @default.
• W1569088697 created "2016-06-24" @default.
• W1569088697 creator A5069978184 @default.
• W1569088697 date "2012-02-10" @default.
• W1569088697 modified "2023-10-03" @default.
• W1569088697 title "The Role of Renin Angiotensin System Inhibitors in Renal Protection: Lessons from Clinical Trials" @default.
• W1569088697 cites W183595628 @default.
• W1569088697 cites W1972358173 @default.
• W1569088697 cites W1975768263 @default.
• W1569088697 cites W1976167638 @default.
• W1569088697 cites W1979363410 @default.
• W1569088697 cites W1984061204 @default.
• W1569088697 cites W1994332748 @default.
• W1569088697 cites W2000154505 @default.
• W1569088697 cites W2001933911 @default.
• W1569088697 cites W2003213033 @default.
• W1569088697 cites W2010407705 @default.
• W1569088697 cites W2011506695 @default.
• W1569088697 cites W2014302862 @default.
• W1569088697 cites W2019310839 @default.
• W1569088697 cites W2026881482 @default.
• W1569088697 cites W2031930369 @default.
• W1569088697 cites W2034269429 @default.
• W1569088697 cites W2034705839 @default.
• W1569088697 cites W2036782549 @default.
• W1569088697 cites W2044773944 @default.
• W1569088697 cites W2045516356 @default.
• W1569088697 cites W2054454858 @default.
• W1569088697 cites W2056976690 @default.
• W1569088697 cites W206681512 @default.
• W1569088697 cites W2070692648 @default.
• W1569088697 cites W2073549750 @default.
• W1569088697 cites W2085580966 @default.
• W1569088697 cites W2085927807 @default.
• W1569088697 cites W2098540575 @default.
• W1569088697 cites W2100409734 @default.
• W1569088697 cites W2107860946 @default.
• W1569088697 cites W2108266187 @default.
• W1569088697 cites W2111511850 @default.
• W1569088697 cites W2118795730 @default.
• W1569088697 cites W2127808551 @default.
• W1569088697 cites W2130229820 @default.
• W1569088697 cites W2133363129 @default.
• W1569088697 cites W2135439806 @default.
• W1569088697 cites W2137177722 @default.
• W1569088697 cites W2137620958 @default.
• W1569088697 cites W2139757550 @default.
• W1569088697 cites W2140563977 @default.
• W1569088697 cites W2143144750 @default.
• W1569088697 cites W2145632481 @default.
• W1569088697 cites W2146582345 @default.
• W1569088697 cites W2165256339 @default.
• W1569088697 cites W2416046640 @default.
• W1569088697 cites W2529012027 @default.
• W1569088697 cites W2615684303 @default.
• W1569088697 cites W2971005880 @default.
• W1569088697 cites W3022958147 @default.
• W1569088697 cites W2003670762 @default.
• W1569088697 cites W2319268509 @default.
• W1569088697 doi "https://doi.org/10.5772/25957" @default.
• W1569088697 hasPublicationYear "2012" @default.
• W1569088697 type Work @default.
• W1569088697 sameAs 1569088697 @default.
• W1569088697 citedByCount "0" @default.
• W1569088697 crossrefType "book-chapter" @default.
• W1569088697 hasAuthorship W1569088697A5069978184 @default.
• W1569088697 hasBestOaLocation W15690886971 @default.
• W1569088697 hasConcept C126322002 @default.
• W1569088697 hasConcept C198710026 @default.
• W1569088697 hasConcept C535046627 @default.
• W1569088697 hasConcept C71924100 @default.
• W1569088697 hasConcept C84393581 @default.
• W1569088697 hasConcept C98274493 @default.
• W1569088697 hasConceptScore W1569088697C126322002 @default.
• W1569088697 hasConceptScore W1569088697C198710026 @default.
• W1569088697 hasConceptScore W1569088697C535046627 @default.
• W1569088697 hasConceptScore W1569088697C71924100 @default.
• W1569088697 hasConceptScore W1569088697C84393581 @default.
• W1569088697 hasConceptScore W1569088697C98274493 @default.
• W1569088697 hasLocation W15690886971 @default.
• W1569088697 hasLocation W15690886972 @default.
• W1569088697 hasOpenAccess W1569088697 @default.
• W1569088697 hasPrimaryLocation W15690886971 @default.
• W1569088697 hasRelatedWork W2044747643 @default.
• W1569088697 hasRelatedWork W2045323206 @default.
• W1569088697 hasRelatedWork W2047608102 @default.
• W1569088697 hasRelatedWork W2068374317 @default.
• W1569088697 hasRelatedWork W2077998387 @default.
• W1569088697 hasRelatedWork W2126797993 @default.
• W1569088697 hasRelatedWork W2149410839 @default.
• W1569088697 hasRelatedWork W2151226843 @default.
• W1569088697 hasRelatedWork W2410599025 @default.
• W1569088697 hasRelatedWork W2418574610 @default.
• W1569088697 isParatext "false" @default.
• W1569088697 isRetracted "false" @default.
• W1569088697 magId "1569088697" @default.
• W1569088697 workType "book-chapter" @default.