FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W4213445874> ?p ?o ?g. }

• W4213445874 endingPage "478" @default.
• W4213445874 startingPage "466" @default.
• W4213445874 abstract "Promoting cardiac lymphangiogenesis exerts beneficial effects for the heart. Exercise can induce physiological cardiac growth with cardiomyocyte hypertrophy and increased proliferation markers in cardiomyocytes. However, it remains unclear whether and how lymphangiogenesis contributes to exercise-induced physiological cardiac growth. We aimed to investigate the role and mechanism of lymphangiogenesis in exercise-induced physiological cardiac growth.Adult C57BL6/J mice were subjected to 3 weeks of swimming exercise to induce physiological cardiac growth. Oral treatment with vascular endothelial growth factor receptor 3 (VEGFR3) inhibitor SAR131675 was used to investigate whether cardiac lymphangiogenesis was required for exercise-induced physiological cardiac growth by VEGFR3 activation. Furthermore, human dermal lymphatic endothelial cell (LEC)-conditioned medium was collected to culture isolated neonatal rat cardiomyocytes to determine whether and how LECs could influence cardiomyocyte proliferation and hypertrophy.Swimming exercise induced physiological cardiac growth accompanied by a remarkable increase of cardiac lymphangiogenesis as evidenced by increased density of lymphatic vessel endothelial hyaluronic acid receptor 1-positive lymphatic vessels in the heart and upregulated LYVE-1 and Podoplanin expressions levels. VEGFR3 was upregulated in the exercised heart, while VEGFR3 inhibitor SAR131675 attenuated exercise-induced physiological cardiac growth as evidenced by blunted myocardial hypertrophy and reduced proliferation marker Ki67 in cardiomyocytes, which was correlated with reduced lymphatic vessel density and downregulated LYVE-1 and Podoplanin in the heart upon exercise. Furthermore, LEC-conditioned medium promoted both hypertrophy and proliferation of cardiomyocytes and contained higher levels of insulin-like growth factor-1 and the extracellular protein Reelin, while LEC-conditioned medium from LECs treated with SAR131675 blocked these effects. Functional rescue assays further demonstrated that protein kinase B (AKT) activation, as well as reduced CCAAT enhancer-binding protein beta (C/EBPβ) and increased CBP/p300-interacting transactivators with E (glutamic acid)/D (aspartic acid)-rich-carboxylterminal domain 4 (CITED4), contributed to the promotive effect of LEC-conditioned medium on cardiomyocyte hypertrophy and proliferation.Our findings reveal that cardiac lymphangiogenesis is required for exercise-induced physiological cardiac growth by VEGFR3 activation, and they indicate that LEC-conditioned medium promotes both physiological hypertrophy and proliferation of cardiomyocytes through AKT activation and the C/EBPβ-CITED4 axis. These results highlight the essential roles of cardiac lymphangiogenesis in exercise-induced physiological cardiac growth." @default.
• W4213445874 created "2022-02-25" @default.
• W4213445874 creator A5000676465 @default.
• W4213445874 creator A5009133589 @default.
• W4213445874 creator A5012318743 @default.
• W4213445874 creator A5036752525 @default.
• W4213445874 creator A5039383725 @default.
• W4213445874 creator A5040774789 @default.
• W4213445874 creator A5063253432 @default.
• W4213445874 creator A5065748034 @default.
• W4213445874 creator A5078882383 @default.
• W4213445874 creator A5085965166 @default.
• W4213445874 creator A5087981019 @default.
• W4213445874 date "2022-07-01" @default.
• W4213445874 modified "2023-10-13" @default.
• W4213445874 title "Lymphangiogenesis contributes to exercise-induced physiological cardiac growth" @default.
• W4213445874 cites W1527522386 @default.
• W4213445874 cites W1568237782 @default.
• W4213445874 cites W1608435511 @default.
• W4213445874 cites W1992532574 @default.
• W4213445874 cites W1999446980 @default.
• W4213445874 cites W1999507007 @default.
• W4213445874 cites W2031050197 @default.
• W4213445874 cites W2031369457 @default.
• W4213445874 cites W2041550708 @default.
• W4213445874 cites W2049708133 @default.
• W4213445874 cites W2065842245 @default.
• W4213445874 cites W2080883510 @default.
• W4213445874 cites W2100347223 @default.
• W4213445874 cites W2108049767 @default.
• W4213445874 cites W2115013104 @default.
• W4213445874 cites W2123933189 @default.
• W4213445874 cites W2129177056 @default.
• W4213445874 cites W2131398028 @default.
• W4213445874 cites W2134737589 @default.
• W4213445874 cites W2139837799 @default.
• W4213445874 cites W2140283135 @default.
• W4213445874 cites W2140725006 @default.
• W4213445874 cites W2148994051 @default.
• W4213445874 cites W2154410414 @default.
• W4213445874 cites W2159745709 @default.
• W4213445874 cites W2168181821 @default.
• W4213445874 cites W2177834950 @default.
• W4213445874 cites W2180050138 @default.
• W4213445874 cites W2194897593 @default.
• W4213445874 cites W2315219108 @default.
• W4213445874 cites W2423259933 @default.
• W4213445874 cites W2486397717 @default.
• W4213445874 cites W2597184639 @default.
• W4213445874 cites W2625006025 @default.
• W4213445874 cites W2747441624 @default.
• W4213445874 cites W2765754947 @default.
• W4213445874 cites W2777827776 @default.
• W4213445874 cites W2800389271 @default.
• W4213445874 cites W2844942161 @default.
• W4213445874 cites W2849590047 @default.
• W4213445874 cites W2896015315 @default.
• W4213445874 cites W2899622393 @default.
• W4213445874 cites W2903729363 @default.
• W4213445874 cites W2904172984 @default.
• W4213445874 cites W2911347271 @default.
• W4213445874 cites W2922429934 @default.
• W4213445874 cites W2992373517 @default.
• W4213445874 cites W3000438116 @default.
• W4213445874 cites W3007965683 @default.
• W4213445874 cites W3041375915 @default.
• W4213445874 cites W3044089250 @default.
• W4213445874 cites W3047038522 @default.
• W4213445874 cites W3112627880 @default.
• W4213445874 cites W3136720998 @default.
• W4213445874 cites W3160798503 @default.
• W4213445874 cites W609959526 @default.
• W4213445874 doi "https://doi.org/10.1016/j.jshs.2022.02.005" @default.
• W4213445874 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/35218948" @default.
• W4213445874 hasPublicationYear "2022" @default.
• W4213445874 type Work @default.
• W4213445874 citedByCount "13" @default.
• W4213445874 countsByYear W42134458742022 @default.
• W4213445874 countsByYear W42134458742023 @default.
• W4213445874 crossrefType "journal-article" @default.
• W4213445874 hasAuthorship W4213445874A5000676465 @default.
• W4213445874 hasAuthorship W4213445874A5009133589 @default.
• W4213445874 hasAuthorship W4213445874A5012318743 @default.
• W4213445874 hasAuthorship W4213445874A5036752525 @default.
• W4213445874 hasAuthorship W4213445874A5039383725 @default.
• W4213445874 hasAuthorship W4213445874A5040774789 @default.
• W4213445874 hasAuthorship W4213445874A5063253432 @default.
• W4213445874 hasAuthorship W4213445874A5065748034 @default.
• W4213445874 hasAuthorship W4213445874A5078882383 @default.
• W4213445874 hasAuthorship W4213445874A5085965166 @default.
• W4213445874 hasAuthorship W4213445874A5087981019 @default.
• W4213445874 hasBestOaLocation W42134458741 @default.
• W4213445874 hasConcept C103041312 @default.
• W4213445874 hasConcept C104317684 @default.
• W4213445874 hasConcept C121608353 @default.
• W4213445874 hasConcept C126322002 @default.
• W4213445874 hasConcept C127561419 @default.
• W4213445874 hasConcept C134018914 @default.

• next