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Cardiovascular Toxicology
Erschienen in: Cardiovascular Toxicology 3/2020

30.09.2019

Oleic Acid Protects from Arsenic-Induced Cardiac Hypertrophy via AMPK/FoxO/NFATc3 Pathway

verfasst von: Jayeeta Samanta, Arunima Mondal, Srimoyee Saha, Santanu Chakraborty, Arunima Sengupta

Erschienen in: Cardiovascular Toxicology | Ausgabe 3/2020

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Abstract

Arsenic toxicity is one of the major environmental problems causing various diseases, cardiovascular disorders is one of them. Several epidemiological studies have shown that arsenic causes cardiac hypertrophy but the detailed molecular mechanism is to be studied yet. This study is designed to determine the molecules involved in the augmentation of arsenic-induced cardiac hypertrophy. Furthermore, the effects of oleic acid on arsenic-induced hypertrophy and cardiac injury have also been investigated. Our results show that arsenic induces cardiac hypertrophy both in vivo in mice and in vitro in rat H9c2 cardiomyocytes. Moreover, arsenic results in decreased activity of AMPK and FoxO1 along with increased NFATc3 expression, a known cardiac hypertrophy inducer. In addition, activation of AMPK and FoxO1 results in reduced NFATc3 expression causing attenuation of arsenic-induced cardiac hypertrophy in H9c2 cells. Interestingly, we have observed that oleic acid helps in ameliorating cardiac hypertrophy in arsenic-exposed mice. Our studies on protection from arsenic-induced cardiac hypertrophy by oleic acid in H9c2 cells shows that oleic acid activates AMPK along with increased nuclear FoxO1 localization, thereby reducing NFATc3 expression and attenuating cardiomyocyte hypertrophy. This study will help in finding out new avenues in treating arsenic-induced cardiac hypertrophy.
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Metadaten
Titel
Oleic Acid Protects from Arsenic-Induced Cardiac Hypertrophy via AMPK/FoxO/NFATc3 Pathway
verfasst von
Jayeeta Samanta
Arunima Mondal
Srimoyee Saha
Santanu Chakraborty
Arunima Sengupta
Publikationsdatum
30.09.2019
Verlag
Springer US
Erschienen in
Cardiovascular Toxicology / Ausgabe 3/2020
Print ISSN: 1530-7905
Elektronische ISSN: 1559-0259
DOI
https://doi.org/10.1007/s12012-019-09550-9

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