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- W3199030343 abstract "Heart failure (HF) is defined as a syndrome caused by an inadequate performance of the heart as a pumping system. Over the course of time this leads to a series of adaptive molecular and interstitial changes, scope of which still remains to be elucidated. The current study utilized immunofluorescence staining technique to examine left atrial (LA) and left ventricular (LV) tissue in high-fat fed pigs which developed metabolic syndrome (MetS) (n=5), as well as in their healthy counterparts (n=5). The goal was to assess the involvement of inflammation (CD163, CD3, CD16), apoptosis (TUNEL), fibrosis (vimentin) and a bile acidactivated receptor (TGR5) in a progressive decrease in cardiac function observed in MetS patients. The results showed a significant increase in the expression of CD163 and CD16 but not CD3 in MetS animals. Further, there was an increase in apoptotic events in MetS animals compared to the control group. Vimentin expression was increased in LV tissue , but not in LA. Finally, a significant increase in TGR5 expression was evident in MetS animals compared to the control group. This study provides an important test of the involvement of bile acids, inflammation, apoptosis and fibrosis in the pathogenesis of HF. Additional studies are needed to elucidate the exact cellular shifts which occur during the HF so new therapeutic options could be developed for this group of patients." @default.
- W3199030343 created "2021-09-27" @default.
- W3199030343 creator A5082904756 @default.
- W3199030343 date "2019-04-02" @default.
- W3199030343 modified "2023-09-25" @default.
- W3199030343 title "Markers of immune cells, apoptosis and fibrosis in a porcine model of metabolic syndrome and a novel involvement of bile acid-activated receptor" @default.
- W3199030343 hasPublicationYear "2019" @default.
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