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- W2945482145 abstract "Abstract Myocardial dysfunction is clinically relevant? repercussion that follows sepsis. Tid 1 protein has been implicated in many biological process. However, the role of Tid 1 in lipopolysaccharide (LPS)‐induced cardiomyocyte hypertrophy and apoptosis remains elusive. In the current research endeavor, we have elucidated the role of Tid1‐S on LPS‐induced cardiac hypertrophy and apoptosis. Interestingly, we found that overexpression of Tid1‐S suppressed TLR‐4, NFATc3, and BNP protein expression which eventually led to inhibition of LPS‐induced cardiac hypertrophy. Moreover, Tid1‐S overexpression attenuated cellular apoptosis and activated survival proteins p‐PI3K and p ser473 Akt. Besides this, Tid1‐S overexpression enhanced ER‐a protein expression. Collectively, our data suggest that Tid1‐S plausibly enhance ER‐a protein and further activate p‐PI3K and p ser473 Akt survival protein expression; which thereby led to attenuation of LPS‐induced apoptosis in cardiomyoblast cells. Interestingly, our data suggest that Tid1‐S is involved in attenuation of cardiomyoblast cells damages induced by LPS." @default.
- W2945482145 created "2019-05-29" @default.
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- W2945482145 date "2019-05-13" @default.
- W2945482145 modified "2023-09-27" @default.
- W2945482145 title "Tid1‐S attenuates LPS‐induced cardiac hypertrophy and apoptosis through ER‐a mediated modulation of p‐PI3K/p‐Akt signaling cascade" @default.
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- W2945482145 doi "https://doi.org/10.1002/jcb.28928" @default.
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