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Researchers found that the filamin A-Drp1 complex mediates mitochondrial fission in a mouse model of hypoxic heart cells. Results show that hypoxic stress brought about the interaction of filamin A with Drp1 and increased Drp1 activity in heart cells. This process led to mitochondrial fragmentation and cell senescence. Further investigation demonstrated that the drug cilnidipine suppressed Drp1-filamin A complex formation and preserved heart cell function.