Title : Study of ER stress and apoptotic proteins in the heart and tumor exposed to doxorubicin.

Pub. Date : 2021 Jun

PMID : 33857568






6 Functional Relationships(s)
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1 Increased DDIT3 in these Dox-treated cardiomyocytes at 24h suggested that increased MitoBax may have promoted ER stress related changes in DDIT3. Doxorubicin DNA damage inducible transcript 3 Homo sapiens
2 Increased DDIT3 in these Dox-treated cardiomyocytes at 24h suggested that increased MitoBax may have promoted ER stress related changes in DDIT3. Doxorubicin DNA damage inducible transcript 3 Homo sapiens
3 In contrast, breast cancer MCF7 cells showed an ER stress response to Dox with increased DDIT3 as early as 3h which may have triggered a positive feedback activation of ATF6 at 12 and 24h and promoted Calnexin. Doxorubicin DNA damage inducible transcript 3 Homo sapiens
4 DDIT3 response in tumors was evoked by Dox, however this response was inversely correlated with increased Bip and Bax expression in hearts from tumor bearing animals. Doxorubicin DNA damage inducible transcript 3 Homo sapiens
5 It is suggested that in Dox-induced cardiotoxicity both mitochondrial and ER stresses play an integral role through a mutual interaction where an inhibition of DDIT3 or Calnexin may also be crucial to achieve Dox resistance in cardiomyocytes. Doxorubicin DNA damage inducible transcript 3 Homo sapiens
6 It is suggested that in Dox-induced cardiotoxicity both mitochondrial and ER stresses play an integral role through a mutual interaction where an inhibition of DDIT3 or Calnexin may also be crucial to achieve Dox resistance in cardiomyocytes. Doxorubicin DNA damage inducible transcript 3 Homo sapiens