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- W2279231838 abstract "Background Adiponectin (APN), an adipose-derived adipokine, alleviates lipopolysaccharide (LPS)-induced injury in multiple organs including hearts although the underlying mechanism in endotoxemia remains elusive. This study was designed to examine the role of adiponectin in LPS-induced cardiac anomalies and inflammation as well as the underlying mechanism with a focus on autophagy — a conserved machinery for bulk degradation of intracellular components. Methods and results Wild-type (WT) and APN−/− mice were challenged with LPS (4 mg/kg) or saline for 6 h. Echocardiography, cardiomyocyte contractile and intracellular Ca2+ properties were evaluated. Markers of autophagy, apoptosis and inflammation including LC3B, p62, Beclin1, AMPK, mTOR, ULK, Caspase 3, Bcl-2, Bax, TLR4, TRAF6, MyD88, IL-1B, TNFα, HMGB1, JNK and IκB were examined using Western blot or RT-PCR. Our results showed that LPS challenge reduced fractional shortening, compromised cardiomyocyte contractile capacity, intracellular Ca2+ handling properties, apoptosis and inflammation, which were accentuated by adiponectin ablation. Adiponectin ablation unmasked the LPS-induced cardiac remodeling (left ventricular end systolic diameter) and prolongation of cell shortening. The detrimental effects of adiponectin ablation were associated with dampened autophagy in response to LPS through an AMPK-mTOR-ULK1-dependent mechanism. In vivo administration of AMPK activator AICAR or the autophagy inducer rapamycin effectively attenuated or obliterated LPS-induced and adiponectin deficiency-accentuated responses without affecting TLR4, TRAF6 and MyD88. Conclusions The findings suggest that AMPK and autophagy may play a permissive role in the adiponectin deficiency-exacerbated cardiac dysfunction, apoptosis and inflammation under LPS challenge possibly at the post-TLR4 receptor level." @default.
- W2279231838 created "2016-06-24" @default.
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- W2279231838 date "2016-04-01" @default.
- W2279231838 modified "2023-10-18" @default.
- W2279231838 title "Permissive role of AMPK and autophagy in adiponectin deficiency-accentuated myocardial injury and inflammation in endotoxemia" @default.
- W2279231838 cites W1567840615 @default.
- W2279231838 cites W1820897387 @default.
- W2279231838 cites W1871378375 @default.
- W2279231838 cites W1969815372 @default.
- W2279231838 cites W1973472942 @default.
- W2279231838 cites W1973573989 @default.
- W2279231838 cites W1976761774 @default.
- W2279231838 cites W1977347871 @default.
- W2279231838 cites W1984191109 @default.
- W2279231838 cites W1985419530 @default.
- W2279231838 cites W1988262777 @default.
- W2279231838 cites W1990840335 @default.
- W2279231838 cites W1992659717 @default.
- W2279231838 cites W1994823455 @default.
- W2279231838 cites W2001761805 @default.
- W2279231838 cites W2013367303 @default.
- W2279231838 cites W2014547268 @default.
- W2279231838 cites W2015633910 @default.
- W2279231838 cites W2025665129 @default.
- W2279231838 cites W2027589607 @default.
- W2279231838 cites W2036903182 @default.
- W2279231838 cites W2040894660 @default.
- W2279231838 cites W2040937158 @default.
- W2279231838 cites W2041168160 @default.
- W2279231838 cites W2044096109 @default.
- W2279231838 cites W2052146004 @default.
- W2279231838 cites W2054203136 @default.
- W2279231838 cites W2054538838 @default.
- W2279231838 cites W2057673608 @default.
- W2279231838 cites W2067937693 @default.
- W2279231838 cites W2076310317 @default.
- W2279231838 cites W2080008726 @default.
- W2279231838 cites W2082170789 @default.
- W2279231838 cites W2082583727 @default.
- W2279231838 cites W2088997040 @default.
- W2279231838 cites W2091034186 @default.
- W2279231838 cites W2096317893 @default.
- W2279231838 cites W2103181489 @default.
- W2279231838 cites W2106174392 @default.
- W2279231838 cites W2107817153 @default.
- W2279231838 cites W2109034822 @default.
- W2279231838 cites W2110263487 @default.
- W2279231838 cites W2117748926 @default.
- W2279231838 cites W2121805726 @default.
- W2279231838 cites W2122408496 @default.
- W2279231838 cites W2122467321 @default.
- W2279231838 cites W2130006068 @default.
- W2279231838 cites W2131438908 @default.
- W2279231838 cites W2136776017 @default.
- W2279231838 cites W2140163252 @default.
- W2279231838 cites W2146124002 @default.
- W2279231838 cites W2147084771 @default.
- W2279231838 cites W2153962342 @default.
- W2279231838 cites W2156545635 @default.
- W2279231838 cites W2157361427 @default.
- W2279231838 cites W2158498082 @default.
- W2279231838 cites W2160659900 @default.
- W2279231838 cites W2164472512 @default.
- W2279231838 cites W2165760729 @default.
- W2279231838 cites W2171004130 @default.
- W2279231838 cites W2330884421 @default.
- W2279231838 cites W3036294205 @default.
- W2279231838 cites W647542028 @default.
- W2279231838 doi "https://doi.org/10.1016/j.yjmcc.2016.02.002" @default.
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