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Conversely, other studies propose that while excessive HO-1 activation might protect against heme-induced oxidative damage, it may also trigger atypical ferroptosis by generating excessive free iron through heme degradation (60)
The ~30-minute half-life of CJC No DAC is a critical feature for physiological research
A combination of sorafenib plus TMZ prevented autophagy induction by sorafenib and promoted apoptosis, mainly by downregulating the expression of Raf, Hsp27, and Hsp72, increasing ER stress [207]
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