The role of TGF-Beta/activin and mTORC2 signaling in cardiac homeostasis
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Cardiovascular disease is the worldwide leading cause of death, especially in elder population. Understanding the mechanisms underlying cardiac aging is crucial for developing effective therapeutic interventions to promote cardiac health. Impaired autophagy and mitochondrial quality control have been previously linked to age-related declines of cardiac function. Yet, how those quality control mechanisms are altered during cardiac aging still remains elusive. Here using Drosophila heart as a model system, we show that activin signaling, a member of TGF-beta superfamily, negatively regulates cardiac autophagy and cardiac health during aging. We found that cardiac-specific knockdown of daw, an activin-like protein in Drosophila, increased cardiac autophagy and prevented age-related cardiac dysfunction, including arrhythmia and bradycardia (slow heart rate). Inhibition of autophagy blocked daw knockdown-mediated cardio-protection. Intriguingly, the key autophagy regulator, mechanistic target of rapamycin complex 1 (mTORC1), was not involved in activin-mediated autophagy. Instead, activin signaling genetically interacted with rictor, the key subunit of mTORC2, to regulate autophagy and cardiac aging. Recently, we found that mTORC2/rictor regulates cardiac mitochondrial fragmentation in Drosophila. Our findings highlight an emerging role of activin signaling and mTORC2 in the regulation of cardiac homeostasis during aging.