These observations align with independent evidence that Opa1 activity is cardioprotective: Opa1-induced mitophagy preserves cardiomyocyte viability after myocardial infarction and is activated by irisin, whereas Opa1 knockdown abolishes irisin’s benefits [52]; and the natural polyphenol punicalagin protects against diabetic cardiomyopathy by promoting Opa1-mediated mitochondrial fusion via a PTP1B-STAT3-Opa1 axis, with Opa1 knockdown abrogating protection [53]. The gene discussed is FNDC5; the disease is diabetic cardiomyopathy.