FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2994828890> ?p ?o ?g. }

• W2994828890 endingPage "32" @default.
• W2994828890 startingPage "23" @default.
• W2994828890 abstract "Type 1 diabetes patients are more prone to have hypertension than healthy individuals, possibly mediated by increased blood pressure (BP) sensitivity to high salt intake. The classical concept proposes that the kidney is central in salt-mediated BP rises, by insufficient renal sodium excretion leading to extracellular fluid volume expansion. Recent animal-derived findings, however, propose a causal role for disturbance of macrophage-mediated lymphangiogenesis. Its relevance for humans, specifically type 1 diabetes patients, is unknown. The present study aimed to assess responses of type 1 diabetes patients to a dietary salt load with regard to BP, extracellular fluid volume (using precise iohexol measurements), and CD163+ macrophage and lymphatic capillary density in skin biopsies. Also, macrophage expression of HLA-DR (a proinflammatory marker) and CD206 (an anti-inflammatory marker) was assessed. Type 1 diabetes patients (n = 8) showed a salt-sensitive BP increase without extracellular fluid volume expansion. Whereas healthy controls (n = 12), who had no BP increase, showed increased skin CD163+ and HLA-DR+ macrophages and dilation of lymphatic skin vasculature after the dietary salt load, these changes were absent (and in case of HLA-DR more heterogenic) in type 1 diabetes patients. In conclusion, we show that salt sensitivity in type 1 diabetes patients cannot be explained by the classical concept of extracellular fluid volume expansion. Rather, we open up a potential role for macrophages and the lymphatic system. Future studies on hypertension and diabetes need to scrutinize these phenomena. Type 1 diabetes patients are more prone to have hypertension than healthy individuals, possibly mediated by increased blood pressure (BP) sensitivity to high salt intake. The classical concept proposes that the kidney is central in salt-mediated BP rises, by insufficient renal sodium excretion leading to extracellular fluid volume expansion. Recent animal-derived findings, however, propose a causal role for disturbance of macrophage-mediated lymphangiogenesis. Its relevance for humans, specifically type 1 diabetes patients, is unknown. The present study aimed to assess responses of type 1 diabetes patients to a dietary salt load with regard to BP, extracellular fluid volume (using precise iohexol measurements), and CD163+ macrophage and lymphatic capillary density in skin biopsies. Also, macrophage expression of HLA-DR (a proinflammatory marker) and CD206 (an anti-inflammatory marker) was assessed. Type 1 diabetes patients (n = 8) showed a salt-sensitive BP increase without extracellular fluid volume expansion. Whereas healthy controls (n = 12), who had no BP increase, showed increased skin CD163+ and HLA-DR+ macrophages and dilation of lymphatic skin vasculature after the dietary salt load, these changes were absent (and in case of HLA-DR more heterogenic) in type 1 diabetes patients. In conclusion, we show that salt sensitivity in type 1 diabetes patients cannot be explained by the classical concept of extracellular fluid volume expansion. Rather, we open up a potential role for macrophages and the lymphatic system. Future studies on hypertension and diabetes need to scrutinize these phenomena. Brief CommentaryEliane F.E. Wenstedt et al. BackgroundAlthough classically, the kidney is supposed to have a central role in the link between salt and hypertension, animal studies suggest a role for macrophages and lymphatic vessels of the skin. Translational SignificanceWe are, to our knowledge, the first to demonstrate that salt induces macrophage influx and lymphatic dilation in the skin of healthy humans, and that this process is disturbed in salt-sensitive type 1 diabetes patients. This agrees with the animal findings that macrophage-mediated lymphangiogenesis is protective against salt-sensitive hypertension development. Future human studies need to scrutinize these phenomena, in order to eventually develop better therapies. Eliane F.E. Wenstedt et al. Although classically, the kidney is supposed to have a central role in the link between salt and hypertension, animal studies suggest a role for macrophages and lymphatic vessels of the skin. We are, to our knowledge, the first to demonstrate that salt induces macrophage influx and lymphatic dilation in the skin of healthy humans, and that this process is disturbed in salt-sensitive type 1 diabetes patients. This agrees with the animal findings that macrophage-mediated lymphangiogenesis is protective against salt-sensitive hypertension development. Future human studies need to scrutinize these phenomena, in order to eventually develop better therapies." @default.
• W2994828890 created "2019-12-26" @default.
• W2994828890 creator A5001169077 @default.
• W2994828890 creator A5003782523 @default.
• W2994828890 creator A5017007651 @default.
• W2994828890 creator A5039164690 @default.
• W2994828890 creator A5040416826 @default.
• W2994828890 creator A5070030883 @default.
• W2994828890 creator A5088263006 @default.
• W2994828890 date "2020-03-01" @default.
• W2994828890 modified "2023-09-25" @default.
• W2994828890 title "Salt-sensitive blood pressure rise in type 1 diabetes patients is accompanied by disturbed skin macrophage influx and lymphatic dilation—a proof-of-concept study" @default.
• W2994828890 cites W1925591757 @default.
• W2994828890 cites W1960544451 @default.
• W2994828890 cites W1971881339 @default.
• W2994828890 cites W1975967728 @default.
• W2994828890 cites W1977440920 @default.
• W2994828890 cites W1992532574 @default.
• W2994828890 cites W1994355238 @default.
• W2994828890 cites W2017821597 @default.
• W2994828890 cites W2029954557 @default.
• W2994828890 cites W2030953256 @default.
• W2994828890 cites W2032541700 @default.
• W2994828890 cites W2038458001 @default.
• W2994828890 cites W20421448 @default.
• W2994828890 cites W2046156532 @default.
• W2994828890 cites W2054969539 @default.
• W2994828890 cites W2060766291 @default.
• W2994828890 cites W2084557056 @default.
• W2994828890 cites W2099540110 @default.
• W2994828890 cites W2107634581 @default.
• W2994828890 cites W2113214088 @default.
• W2994828890 cites W2115654703 @default.
• W2994828890 cites W2116625819 @default.
• W2994828890 cites W2118463160 @default.
• W2994828890 cites W2120061572 @default.
• W2994828890 cites W2126992402 @default.
• W2994828890 cites W2129220013 @default.
• W2994828890 cites W2134592373 @default.
• W2994828890 cites W2152405846 @default.
• W2994828890 cites W2159560463 @default.
• W2994828890 cites W2165109678 @default.
• W2994828890 cites W2170069518 @default.
• W2994828890 cites W2344803633 @default.
• W2994828890 cites W2505661818 @default.
• W2994828890 cites W2544157559 @default.
• W2994828890 cites W2585705787 @default.
• W2994828890 cites W2598538875 @default.
• W2994828890 cites W2741123422 @default.
• W2994828890 cites W2763571621 @default.
• W2994828890 cites W2767770684 @default.
• W2994828890 cites W2790127876 @default.
• W2994828890 cites W2790874263 @default.
• W2994828890 cites W2805950251 @default.
• W2994828890 cites W2887058054 @default.
• W2994828890 cites W2916293401 @default.
• W2994828890 doi "https://doi.org/10.1016/j.trsl.2019.12.001" @default.
• W2994828890 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/31883728" @default.
• W2994828890 hasPublicationYear "2020" @default.
• W2994828890 type Work @default.
• W2994828890 sameAs 2994828890 @default.
• W2994828890 citedByCount "8" @default.
• W2994828890 countsByYear W29948288902020 @default.
• W2994828890 countsByYear W29948288902021 @default.
• W2994828890 countsByYear W29948288902022 @default.
• W2994828890 countsByYear W29948288902023 @default.
• W2994828890 crossrefType "journal-article" @default.
• W2994828890 hasAuthorship W2994828890A5001169077 @default.
• W2994828890 hasAuthorship W2994828890A5003782523 @default.
• W2994828890 hasAuthorship W2994828890A5017007651 @default.
• W2994828890 hasAuthorship W2994828890A5039164690 @default.
• W2994828890 hasAuthorship W2994828890A5040416826 @default.
• W2994828890 hasAuthorship W2994828890A5070030883 @default.
• W2994828890 hasAuthorship W2994828890A5088263006 @default.
• W2994828890 hasBestOaLocation W29948288901 @default.
• W2994828890 hasConcept C126322002 @default.
• W2994828890 hasConcept C134018914 @default.
• W2994828890 hasConcept C142724271 @default.
• W2994828890 hasConcept C181152851 @default.
• W2994828890 hasConcept C185592680 @default.
• W2994828890 hasConcept C203014093 @default.
• W2994828890 hasConcept C2113261 @default.
• W2994828890 hasConcept C2777180221 @default.
• W2994828890 hasConcept C28406088 @default.
• W2994828890 hasConcept C55493867 @default.
• W2994828890 hasConcept C555293320 @default.
• W2994828890 hasConcept C71924100 @default.
• W2994828890 hasConcept C84393581 @default.
• W2994828890 hasConceptScore W2994828890C126322002 @default.
• W2994828890 hasConceptScore W2994828890C134018914 @default.
• W2994828890 hasConceptScore W2994828890C142724271 @default.
• W2994828890 hasConceptScore W2994828890C181152851 @default.
• W2994828890 hasConceptScore W2994828890C185592680 @default.
• W2994828890 hasConceptScore W2994828890C203014093 @default.
• W2994828890 hasConceptScore W2994828890C2113261 @default.
• W2994828890 hasConceptScore W2994828890C2777180221 @default.
• W2994828890 hasConceptScore W2994828890C28406088 @default.
• W2994828890 hasConceptScore W2994828890C55493867 @default.

• next