FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2891769573> ?p ?o ?g. }

• W2891769573 abstract "Background Activin receptor‐like kinase 4 ( ALK 4) is highly expressed in mammal heart. Atrial fibrillation ( AF ) is closely related to ventricular pressure overload. Because pressure overload increases atrial pressure and leads to atrial remodeling, it would be informative to know whether ALK 4 exerts potential effects on atrial remodeling and AF vulnerability in a pressure‐overload model. Methods and Results Wild‐type littermates and ALK 4 +/− mice were subjected to abdominal aortic constriction or a sham operation. After 4 or 8 weeks, echocardiographic and hemodynamic measurements were performed, and inducibility of AF was tested. The hearts were divided into atria and ventricles and then were fixed in formalin for staining, or they were weighted and snap‐frozen for quantitative real‐time polymerase chain reaction and Western blot analysis. Compared with wild‐type littermates, ALK 4 +/− mice demonstrated a similar extent of atrial hypertrophy but significantly suppressed atrial fibrosis at 8 weeks post–abdominal aortic constriction. ALK 4 haplodeficiency partially blocked abdominal aortic constriction–induced upregulation of monocyte chemotactic protein 1 and interleukin‐6, and the increased chemotaxin of macrophages. ALK 4 haplodeficiency also blunted a reduction of connexin 40 and redistribution of connexin 43 from the intercalated disk to the lateral membranes, thereby improving localized conduction abnormalities. Meanwhile, ALK 4 haplodeficiency inhibited abdominal aortic constriction–induced decreased I N a , I C a‐L and I K 1 densities as well as the accompanying action potential duration shortening. Mechanistically, ALK 4 haploinsufficiency resulted in the suppression of Smad2/3 activity in this model. Conclusions Our results demonstrate that ALK 4 haplodeficiency ameliorates atrial remodeling and vulnerability to AF in a pressure‐overload model through inactivation of the Smad2/3 pathway, suggesting that ALK 4 might be a potential therapeutic target in combating pressure overload–induced AF ." @default.
• W2891769573 created "2018-09-27" @default.
• W2891769573 creator A5036885388 @default.
• W2891769573 creator A5042050339 @default.
• W2891769573 creator A5046225712 @default.
• W2891769573 creator A5046409597 @default.
• W2891769573 creator A5063688245 @default.
• W2891769573 creator A5065526643 @default.
• W2891769573 creator A5066034390 @default.
• W2891769573 creator A5084945548 @default.
• W2891769573 creator A5088499288 @default.
• W2891769573 date "2018-08-21" @default.
• W2891769573 modified "2023-10-12" @default.
• W2891769573 title "Activin Receptor‐Like Kinase 4 Haplodeficiency Mitigates Arrhythmogenic Atrial Remodeling and Vulnerability to Atrial Fibrillation in Cardiac Pathological Hypertrophy" @default.
• W2891769573 cites W1506429854 @default.
• W2891769573 cites W1637524329 @default.
• W2891769573 cites W1850125129 @default.
• W2891769573 cites W1982983732 @default.
• W2891769573 cites W1983741639 @default.
• W2891769573 cites W1994069214 @default.
• W2891769573 cites W2003728637 @default.
• W2891769573 cites W2006570186 @default.
• W2891769573 cites W2007309690 @default.
• W2891769573 cites W20074729 @default.
• W2891769573 cites W2030127516 @default.
• W2891769573 cites W2040399166 @default.
• W2891769573 cites W2041137798 @default.
• W2891769573 cites W2064311777 @default.
• W2891769573 cites W2071675848 @default.
• W2891769573 cites W2077088300 @default.
• W2891769573 cites W2087873914 @default.
• W2891769573 cites W2088163803 @default.
• W2891769573 cites W2091365349 @default.
• W2891769573 cites W2095813633 @default.
• W2891769573 cites W2102051477 @default.
• W2891769573 cites W2103042473 @default.
• W2891769573 cites W2114512872 @default.
• W2891769573 cites W2119960643 @default.
• W2891769573 cites W2132572082 @default.
• W2891769573 cites W2135535764 @default.
• W2891769573 cites W2138991213 @default.
• W2891769573 cites W2167423131 @default.
• W2891769573 cites W2170969868 @default.
• W2891769573 cites W2194428021 @default.
• W2891769573 cites W2233003736 @default.
• W2891769573 cites W2233015826 @default.
• W2891769573 cites W2273608205 @default.
• W2891769573 cites W2340953831 @default.
• W2891769573 cites W2472710576 @default.
• W2891769573 cites W2486230686 @default.
• W2891769573 cites W2491103610 @default.
• W2891769573 cites W2503685584 @default.
• W2891769573 cites W2538023870 @default.
• W2891769573 cites W2573729299 @default.
• W2891769573 cites W2580844460 @default.
• W2891769573 cites W2588604744 @default.
• W2891769573 cites W2610373723 @default.
• W2891769573 cites W2612172550 @default.
• W2891769573 cites W2618701383 @default.
• W2891769573 cites W2646125913 @default.
• W2891769573 cites W2647098128 @default.
• W2891769573 cites W2698675912 @default.
• W2891769573 cites W2739133817 @default.
• W2891769573 cites W2751547438 @default.
• W2891769573 cites W2757004157 @default.
• W2891769573 cites W2772664156 @default.
• W2891769573 cites W2792289288 @default.
• W2891769573 cites W2891769573 @default.
• W2891769573 doi "https://doi.org/10.1161/jaha.118.008842" @default.
• W2891769573 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6201394" @default.
• W2891769573 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30369314" @default.
• W2891769573 hasPublicationYear "2018" @default.
• W2891769573 type Work @default.
• W2891769573 sameAs 2891769573 @default.
• W2891769573 citedByCount "17" @default.
• W2891769573 countsByYear W28917695732017 @default.
• W2891769573 countsByYear W28917695732019 @default.
• W2891769573 countsByYear W28917695732020 @default.
• W2891769573 countsByYear W28917695732021 @default.
• W2891769573 countsByYear W28917695732022 @default.
• W2891769573 countsByYear W28917695732023 @default.
• W2891769573 crossrefType "journal-article" @default.
• W2891769573 hasAuthorship W2891769573A5036885388 @default.
• W2891769573 hasAuthorship W2891769573A5042050339 @default.
• W2891769573 hasAuthorship W2891769573A5046225712 @default.
• W2891769573 hasAuthorship W2891769573A5046409597 @default.
• W2891769573 hasAuthorship W2891769573A5063688245 @default.
• W2891769573 hasAuthorship W2891769573A5065526643 @default.
• W2891769573 hasAuthorship W2891769573A5066034390 @default.
• W2891769573 hasAuthorship W2891769573A5084945548 @default.
• W2891769573 hasAuthorship W2891769573A5088499288 @default.
• W2891769573 hasBestOaLocation W28917695731 @default.
• W2891769573 hasConcept C126322002 @default.
• W2891769573 hasConcept C134018914 @default.
• W2891769573 hasConcept C164705383 @default.
• W2891769573 hasConcept C167414201 @default.
• W2891769573 hasConcept C174940676 @default.
• W2891769573 hasConcept C2778271984 @default.
• W2891769573 hasConcept C2779161974 @default.
• W2891769573 hasConcept C2780559512 @default.

• next