How does disrupted MCL-1/ACSL1 interaction contribute to cardiac toxicity of MCL-1 inhibitors in clinical trials?

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Description

The authors suggest that disruption of MCL-1’s metabolic function may cause cardiac toxicities observed with MCL-1 inhibitors, but the causal relationship and underlying pathophysiology are not established. This gap is critical for developing safer MCL-1-targeted therapeutics.

Gap type: open_question Source paper: Anti-apoptotic MCL-1 promotes long-chain fatty acid oxidation through interaction with ACSL1. (None, None, PMID:38503284)

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