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Considering that apoptosis contributes minimally to human heart failure, with only 80–250 cardiomyocytes per 100,000 affected, non-apoptotic cell death mechanisms, including ferroptosis, gain prominence in this context [12, 13]
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The liver decides whether to burn those fats for energy, package them into lipoproteins for transport to other tissues, or re-esterify them for storage
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