FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W1823641798> ?p ?o ?g. }

• W1823641798 endingPage "606" @default.
• W1823641798 startingPage "592" @default.
• W1823641798 abstract "Aging is associated with myocardial dysfunction although the underlying mechanism is unclear. AMPK, a key cellular fuel sensor for energy metabolism, is compromised with aging. This study examined the role of AMPK deficiency in aging-associated myocardial dysfunction. Young or old wild-type (WT) and transgenic mice with overexpression of a mutant AMPK α2 subunit (kinase dead, KD) were used. AMPK α isoform activity, myocardial function and morphology were examined. DCF and JC-1 fluorescence probes were employed to quantify reactive oxygen species (ROS) and mitochondrial membrane potential (ΔΨm), respectively. KD mice displayed significantly reduced α2 but not α1 AMPK isoform activity at both ages with a greater effect at old age. Aging itself decreased α1 isoform activity. Cardiomyocyte contractile function, intracellular Ca2+ handling, and SERCA2a levels were compromised with aging, the effects of which were exacerbated by AMPK deficiency. H&E staining revealed cardiomyocyte hypertrophy with aging, which was more pronounced in KD mice. TEM micrographs displayed severe disruption of mitochondrial ultrastructure characterized by swollen, irregular shape and disrupted cristae in aged KD compared with WT mice. Aging enhanced ROS production and reduced ΔΨm, the effects of which were accentuated by AMPK deficiency. Immunoblotting data depicted unchanged Akt phosphorylation and a significant decrease in mitochondrial biogenesis cofactor PGC-1α in aged groups. AMPK deficiency but not aging decreased the phosphorylation of ACC and eNOS. Expression of membrane Glut4 and HSP90 was decreased in aged KD mice. Moreover, treatment of the AMPK activator metformin attenuated aging-induced cardiomyocyte contractile defects. Collectively, our data suggest a role for AMPK deficiency in aging-induced cardiac dysfunction possibly through disrupted mitochondrial function and ROS production." @default.
• W1823641798 created "2016-06-24" @default.
• W1823641798 creator A5007706452 @default.
• W1823641798 creator A5011129666 @default.
• W1823641798 creator A5015953462 @default.
• W1823641798 creator A5058490930 @default.
• W1823641798 creator A5064803348 @default.
• W1823641798 creator A5074270918 @default.
• W1823641798 creator A5089191965 @default.
• W1823641798 date "2010-04-01" @default.
• W1823641798 modified "2023-10-14" @default.
• W1823641798 title "AMP-activated protein kinase deficiency exacerbates aging-induced myocardial contractile dysfunction" @default.
• W1823641798 cites W1565979608 @default.
• W1823641798 cites W1962360047 @default.
• W1823641798 cites W1968340356 @default.
• W1823641798 cites W1975724219 @default.
• W1823641798 cites W1980608195 @default.
• W1823641798 cites W1981785619 @default.
• W1823641798 cites W1997580795 @default.
• W1823641798 cites W2000776278 @default.
• W1823641798 cites W2002806885 @default.
• W1823641798 cites W2005915142 @default.
• W1823641798 cites W2007256995 @default.
• W1823641798 cites W2016640448 @default.
• W1823641798 cites W2021399218 @default.
• W1823641798 cites W2027237238 @default.
• W1823641798 cites W2033539191 @default.
• W1823641798 cites W2039167216 @default.
• W1823641798 cites W2042444876 @default.
• W1823641798 cites W2046490985 @default.
• W1823641798 cites W2056642306 @default.
• W1823641798 cites W2068820862 @default.
• W1823641798 cites W2073342055 @default.
• W1823641798 cites W2073534977 @default.
• W1823641798 cites W2077645437 @default.
• W1823641798 cites W2079479408 @default.
• W1823641798 cites W2083025420 @default.
• W1823641798 cites W2087766892 @default.
• W1823641798 cites W2097668381 @default.
• W1823641798 cites W2099962252 @default.
• W1823641798 cites W2100580464 @default.
• W1823641798 cites W2105927334 @default.
• W1823641798 cites W2109693559 @default.
• W1823641798 cites W2110292185 @default.
• W1823641798 cites W2112133879 @default.
• W1823641798 cites W2112244734 @default.
• W1823641798 cites W2114349736 @default.
• W1823641798 cites W2124536446 @default.
• W1823641798 cites W2129917446 @default.
• W1823641798 cites W2133867913 @default.
• W1823641798 cites W2138812648 @default.
• W1823641798 cites W2139638456 @default.
• W1823641798 cites W2141718522 @default.
• W1823641798 cites W2147594695 @default.
• W1823641798 cites W2149568634 @default.
• W1823641798 cites W2153903825 @default.
• W1823641798 cites W2156029342 @default.
• W1823641798 cites W2160234571 @default.
• W1823641798 cites W2162378911 @default.
• W1823641798 cites W2165826818 @default.
• W1823641798 cites W2169384785 @default.
• W1823641798 cites W2170880090 @default.
• W1823641798 cites W2176414067 @default.
• W1823641798 doi "https://doi.org/10.1111/j.1474-9726.2010.00586.x" @default.
• W1823641798 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2910211" @default.
• W1823641798 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/20477759" @default.
• W1823641798 hasPublicationYear "2010" @default.
• W1823641798 type Work @default.
• W1823641798 sameAs 1823641798 @default.
• W1823641798 citedByCount "109" @default.
• W1823641798 countsByYear W18236417982012 @default.
• W1823641798 countsByYear W18236417982013 @default.
• W1823641798 countsByYear W18236417982014 @default.
• W1823641798 countsByYear W18236417982015 @default.
• W1823641798 countsByYear W18236417982016 @default.
• W1823641798 countsByYear W18236417982017 @default.
• W1823641798 countsByYear W18236417982018 @default.
• W1823641798 countsByYear W18236417982019 @default.
• W1823641798 countsByYear W18236417982020 @default.
• W1823641798 countsByYear W18236417982021 @default.
• W1823641798 countsByYear W18236417982022 @default.
• W1823641798 countsByYear W18236417982023 @default.
• W1823641798 crossrefType "journal-article" @default.
• W1823641798 hasAuthorship W1823641798A5007706452 @default.
• W1823641798 hasAuthorship W1823641798A5011129666 @default.
• W1823641798 hasAuthorship W1823641798A5015953462 @default.
• W1823641798 hasAuthorship W1823641798A5058490930 @default.
• W1823641798 hasAuthorship W1823641798A5064803348 @default.
• W1823641798 hasAuthorship W1823641798A5074270918 @default.
• W1823641798 hasAuthorship W1823641798A5089191965 @default.
• W1823641798 hasBestOaLocation W18236417981 @default.
• W1823641798 hasConcept C11960822 @default.
• W1823641798 hasConcept C126322002 @default.
• W1823641798 hasConcept C134018914 @default.
• W1823641798 hasConcept C161573976 @default.
• W1823641798 hasConcept C2776188179 @default.
• W1823641798 hasConcept C2776780712 @default.
• W1823641798 hasConcept C2777229759 @default.

• next